The Dirty Dozen

THE DIRTY DOZEN:
Toxic Chemicals and

the Earth’s Future
Bruce E. Johansen
PRAEGER
THE DIRT Y DOZEN
THE DIR T Y
DOZEN
Toxic Chemicals and
the Earth’s Future
Bruce E. Johansen
Library of Congress Cataloging-in-Publication Data
Johansen, Bruce E. (Bruce Elliott), 1950–

The dirty dozen : toxic chemicals and the earth’s future / Bruce E.
Johansen
p. cm.
Includes bibliographical references and index.
ISBN 0–275–97702–1 (alk. paper)
1. Organochlorine compounds—Environmental aspects.
2. Persistent pollutants—Environmental aspects. 3. Organochlorine
compounds—Health aspects. 4. Persistent pollutants—Health
aspects. I. Title.
TD196.C5J65 2003
363.738⬘4—dc21 2002029872
British Library Cataloguing in Publication Data is available.
Copyright 䉷 2003 by Bruce E. Johansen
All rights reserved. No portion of this book may be

reproduced, by any process or technique, without the
express written consent of the publisher.
Library of Congress Catalog Card Number: 2002029872

ISBN: 0–275–97702–1
First published in 2003
Praeger Publishers, 88 Post Road West, Westport, CT 06881

An imprint of Greenwood Publishing Group, Inc.
www.praeger.com
Printed in the United States of America
The paper used in this book complies with the

Permanent Paper Standard issued by the National
Information Standards Organization (Z39.48–1984).
10 9 8 7 6 5 4 3 2 1
Copyright Acknowledgments
The author and publisher gratefully acknowledge permission for use of
the following material:
Excerpts from the personal communications of Sheila Watt-Cloutier.
Excerpts from the personal communications of Barbara Alice Mann.
Contents
Preface vii
Introduction 1
1. Persistent Organic Pollutants: The Basics 11

2. “We Feel like an Endangered Species”: Toxics in the
Arctic 47
3. CFCs, Global Warming, and Ozone Depletion 77
4. The Chemical Industry, Nonwhite Communities, and the
Third World 107
5. Belugas with Tumors: The Toxic Toll on Animals 133
6. End of the Line: The Dirty Dozen and Human Health 165
7. Toxic Barbie? Not Your Great-Grandmother’s Estrogen 199
8. Solutions: Public Policy Issues 229
Glossary 249
Selected Bibliography 253
Index 291
Preface
I was introduced to the human and natural toll of persistent organic

pollutants in a scholarly way via e-mailed descriptions of a press
conference held in New York City with, among others, the eminent
ecologist Barry Commoner, and Sheila Watt-Cloutier, Canadian
president of the Inuit Circumpolar Conference, October 3, 2000
(Commoner 1966, 1971, 1990).
Watt-Cloutier herself had become a major driving force behind the
negotiation of the Stockholm Convention that will eventually ban
the most widely used and dangerous organochlorines. Her testi-
mony about the toll of persistent organic pollutants on the Inuit and
Arctic animals haunted me as I plunged deeper into the subject
during ensuing months. Ten months later, we met on Baffin Island,
at Iqaluit, to discuss the toll of persistent organic pollutants, as well
as global warming, on her people.
Commoner’s study included precise identification of dioxin
sources across North America that were poisoning the Inuit, and
Watt-Cloutier warned that the toxicity that befalls the Inuit today
could afflict all humankind a few generations hence if the produc-
tion of dioxins, polyvinyl chloride (PCBs), and other bioaccumulat-
ing organochlorines is not stopped. Some of the sources that the
study identified were only a few miles from my home in Omaha,
Nebraska, where my concern about organochlorines had been
stirred informally and anecdotally for many years by the levels of
agricultural pesticide and herbicide runoff in our municipal water.
Levels were high enough to prompt my wife to order bottled water
when we had infants in the house.
viii Preface
Viewed from the top of the world, where ocean and wind currents
cause the dirty dozen to concentrate, the arrival of persistent or-
ganic pollutants is a direct threat to a way of life based on Arctic
animal protein. Given atmospheric and biological circumstances,
the Arctic—still a pristine place in many non-Inuit imaginations—
has become a testing ground for the perils of environmental toxi-
cology. As Watt-Cloutier observes in chapter 2, the lives of the Inuit
have been imperiled by persistent organic pollutants in a way that
many of the chemicals’ producers and consumers have only slowly
come to realize.
After hearing from Watt-Cloutier that many Inuit mothers were
refraining from breast-feeding their children because of dioxins,
PCBs (polychlorinated biphenyls), and other chemicals in their food
chain, I set out to compose an account of these toxins that would
be accessible to undergraduate students and other members of
the reading public in the areas of North America where they are
produced, before their transport by atmospheric and oceanic cir-
culations to the Arctic. I began with the dirty dozen, the twelve
substances that have been short-listed for elimination by the Stock-
holm Convention, including the organochlorine pesticides (DDT,
chlordane, mirex, hexachlorobenzene, endrin, aldrin, dieldrin, tox-
aphene, heptachlor), as well as industrial chemicals (including
PCBs and the supertoxic dioxins and furans). Because some of
these substances (notably the PCBs and dioxins) are actually fam-
ilies comprising hundreds of chemicals, this list could just as aptly
be called the dirty hundreds as the dirty dozen.
I read with astonishment Watt-Cloutier’s descriptions of how Inuit
children were being injured by exposure to PCBs and dioxins, and
of Inuit mothers’ toxic breast milk. Hers was an account that very
few people in North America had heard at that time. Most of my
undergraduate students in communication professed ignorance of
the chemicals afflicting the Arctic, such as PCBs and dioxins. Only
when I mentioned Agent Orange did I receive a knowing nod from
students who, for the most part, dread our required courses in basic
sciences, including chemistry.
Unlike the debate over global warming, about which President
George W. Bush has played antagonist to most of the world, the
evidence of damage (past and potential) of persistent organic pol-
lutants is so incontrovertible that even the United States has
pledged support of the Stockholm Convention. What remains to be
Preface ix
negotiated are the methods and pace of their elimination, first in

manufacturing and then, as the twenty-first century passes, in our
atmosphere, oceans, and food web.
ACKNOWLEDGMENTS
Thanks are due the staff of the Progressive, especially its editor-
in-chief Matthew Rothschild, for publishing an article that started
me down the road to this book (Johansen 2000). The Progressive
also paid for a trip to the Arctic during the summer of 2001 that
allowed me to meet Sheila Watt-Cloutier personally. I owe her my
thanks for arranging interviews that allowed me to witness the per-
ils of industry for today’s Inuit—not only the ravages of dioxins and
PCBs, but also the accelerating pace of global warming that is de-
stroying the area’s ice-based ecology.
I also owe a debt of gratitude, as always, to the staff of University
of Nebraska at Omaha Interlibrary Loan, and to Deborah Smith-
Howell, Communication Department chairwoman, for partial relief
from teaching duties that has allowed me time to research this and
other books and articles. This book also has benefited immensely
from the comments of an anonymous peer reviewer who provided a
rigorous red inking of the manuscript before it began its sojourn
through production at Greenwood Press. At the press, thanks also
are due my editors on this volume, Cynthia Harris and Heather Ru-
land Staines.
Finally, many thanks to my wife, Pat Keiffer, for her intellectual
stimulation, advice, support, encouragement, and wonderful din-
ners following long days of slogging through some very complex,
sometimes depressing, but very necessary information that will be
vital to the future of the Inuit—and to the environmental health of
the entire world.
REFERENCES
Commoner, Barry. 1966. Science and Survival. New York: Viking Press.
———. 1971. The Closing Circle: Nature, Man, and Technology. New York:
Knopf.
———. 1990. Making Peace with the Planet. New York: Pantheon Books.
Johansen, Bruce E. 2000. “Pristine No More: The Arctic, Where Mother’s
Milk Is Toxic.” Progressive, December, 27–29.
Introduction
Our economic system has been very good at developing ways to

exploit chemistry for human welfare and profit. It has been less
sagacious at anticipating, detecting, and dealing with chemistry’s
unintended consequences. In our economy (at least until recent
times) novelty, convenience, and profit came first, and environmen-
tal questions often were asked later, if ever. Medical testing often
occurs only after effects have become evident anecdotally.
During 1928, for example, the New York Times (March 15, 1929)
carried on its front page a report headlined “Professor, P.Q. Card
Pictures Frocks of Asbestos.” Nine days later, on page 2 of the Sun-
day Times’s section 11, a feature foretold the use of asbestos in
high-fashion dresses. At about the same time, other fashion-
conscious consumers were buying wristwatches with radioactive
radium dials that shone in the dark. Two decades later, uranium-
mining companies in New Mexico and Arizona sent Navajos into the
earth to mine radioactive uranium with no protective gear, as if it
was coal. During their lunch breaks, the miners washed their food
down with swigs of radioactive water that flowed through the mines.
Lacking toilet paper, miners sometimes cleaned themselves with
wads of radioactive yellowcake. Three and four decades later, a large
number of former uranium miners died of lung cancer in an area
where the disease had been nearly unknown.
Earthwide, human-induced pollution is unique to our time. Hu-
man beings, as a species, no longer foul only small parts of the Earth
(such as specific cities or bodies of water) at a time. Tom Brokaw’s
“Greatest Generation” did, indeed, win World War II. The irony is
that the same generation also gave us a wonder-world of synthetic
2 The Dirty Dozen
chlorinated hydrocarbons that have left a devastating environmen-

tal heritage. Each of these chemicals is built on a chlorine base. “The
chlorine gas produced by the chemical industry is violently reactive,
combining quickly and promiscuously with any organic matter with
which it comes in contact to produce a new family of compounds
called organochlorines” (Thornton 2000, 203–4).
Synthetic organochlorines such as dioxins and polychlorinated
biphenyls (PCBs) are a perfect vehicle for worldwide pollution be-
cause they ignore virtually all boundaries, natural and artificial. We
are now chemical neighbors of the Inuit and polar bears in the Arc-
tic, the whales in the sea, and the penguins of Antarctica. All of us
now carry in our bodies trace amounts of some of the most potent
toxins created by human industrial ingenuity.
These chemicals bioaccumulate (intensify in potency) along the
food chain, sometimes to thousands of times their original toxicity,
posing special perils to animals, including human beings, who eat
meat and fish. Problems related to their toxicity are especially acute
in places, such as the polar regions, where currents in the atmo-
sphere and oceans cause organochlorines to accumulate. The
bull’s-eye on our industrial chemical target has become mothers of
Inuit children who now pass along their bioaccumulating toxic bur-
den to their children in breast milk. The Arctic remains pristine only
to those who know nothing of how toxic synthetic poisons behave.
Today, organochlorines produced for commerce and those cre-
ated unintentionally can be found in the air, lakes, oceans, soils,
sediments, and animals, including humans, in every region of the
planet. The effects of these substances on the environment, par-
ticularly on human health, “has emerged as one of the most com-
pelling scientific, political and economic issues of our time” (Allsopp,
Costner, and Johnston, 1995). Readers of this book may visit vil-
lages in the Arctic west of Greenland, where people have higher con-
centrations of PCBs than anywhere else on Earth (except victims of
industrial accidents). They are at the top of a food chain composed
mainly of PCB-laced polar bears, seals, and other animals.
Persistent organic pollutants (POPs), of which PCBs are one ex-
ample, are not soluble in water. They dissolve readily, however, in
fats and oils. Because of their resistance to degradation and affinity
for fat, POPs accumulate in the body fat of living organisms and
become more concentrated as they move from one creature to an-
other onward and upward in the food chain. In this way, extremely
Introduction 3
small levels of such contaminants in water or soil can magnify into

a significant hazard to predators who feed at the top of the food web
such as dolphins, polar bears, herring gulls, and human beings. In
Lake Ontario, for example, the tissue of herring gulls may contain
25 million times the concentration of PCBs found in the lake’s water.
Imagine being a polar bear in today’s world: your body is bioac-
cumulating enough synthetic toxins in your body fat to imperil re-
production in coming generations. You wake from a long winter’s
sleep hungry for seal meat, but you find that the ice shelf that once
brought you food has moved offshore, a result of global warming. If
you are close to a human settlement (such as Churchill, Manitoba,
where polar bears have often foraged in recent years), you wander
into town looking for something to eat, miserably out of sync with
this brave new world. You may not realize it, but a developing hole
in the Arctic ozone layer soon may give you skin cancer.
We have had nearly four decades to tally the worldwide toll of or-
ganochlorines since Rachel Carson’s (1962b, 7) statement, in Silent
Spring, that
The chemicals to which life is asked to make its adjustment are no longer
merely the calcium and silica and copper and all the rest of the minerals
washed out of the rocks and carried in rivers to the sea; they are the syn-
thetic creations of man’s inventive mind, brewed in his laboratories, and
having no counterparts in nature.
For the first time in the history of the world, Carson (1962a, 24)
wrote,
Every human being is now subjected to contact with dangerous chemicals,

from the moment of conception until death. In the less than two decades of
their use, the synthetic pesticides have been so thoroughly distributed
throughout the animate and inanimate world that they occur virtually
everywhere.
During the early twentieth century, human beings learned to syn-

thesize chemicals for the first time on a scale and with a practicality
that has since mightily shaped our commerce. For the first time,
many thousands of synthetic substances were discharged into the
environment with little forethought regarding how they might in-
teract with the preexisting biological landscape. These chemicals
are some of the most potent toxins ever developed. For example, one
drop of dioxin, spread among 1,200 people, could kill all of them
(Cook and Kaufman 1982, 1).
4 The Dirty Dozen
The Dirty Dozen begins in chapter 1 with a basic primer on syn-

thetic organochlorines—what they are, how they originated, and
why they are dangerous. Chapter 1 is organized around a historical
narrative of synthetic chemistry, its uses, and its abuses, including
a number of notable accidents after which scientists learned, often
for the first time, what synthetic organochlorines can do to human
and animal biology. Chapter 2 focuses on a half-dozen areas in
which persistent organic pollutants have had a dramatic impact.
This account begins in the Arctic with Inuit mothers who have
learned they may be poisoning the next generation by feeding them
POP-laced breast milk. Chapter 3 is on the chemical legacy that
connects the depletion of stratospheric ozone with global warming.
The interlocking chemistry of stratospheric ozone depletion and
global warming also has implications for the Inuit, because the
ozone layer has been rapidly thinning over their heads.
Chapter 4 introduces, through a number of local reports, the toll
of synthetic toxins on minority ethnic groups in the United States.
We begin with the Rosebud Sioux of South Dakota and continue to
Akwesasne, land of the toxic turtles, a Mohawk reservation bisected
by the U.S.–Canada border. The chapter concludes in “Cancer
Alley,” Louisiana, along the Mississippi River between Baton Rouge
and New Orleans, with its ranks of petrochemical manufacturing
plants.
Chapters 5, 6, and 7 of this book are devoted to a survey of ways
in which persistent organic pollutants inflict physiological damage
on humans and other animals. The reader should be prepared to
enter a brave new chemical world in which vultures in India die from
eating contaminated carrion, a world where being toxic may save
the whales, at least for a few generations. It is a world of belugas
with tumors and sterile bald eagles.
Chapter 8 of The Dirty Dozen focuses specifically on estrogenic
effects that are creating a notable amount of sexual confusion. The
reader may be startled to learn that, in a world of burgeoning hu-
manity, sperm counts have declined as much as 50 percent in 50
years. On this journey, readers should be prepared to meet polar
bears, frogs, and alligators with two sets of sexual organs. Such
hormone-disrupting persistent contaminants can be hazardous at
extremely low doses and pose a particular danger to offspring ex-
posed in the womb. During prenatal life, endocrine disrupters can
alter development and undermine the ability to learn, to fight off
disease, and to reproduce.
Introduction 5
Chapter 8 surveys public-policy solutions to the POP dilemma.

An international ban of the dirty dozen was signed in Stockholm
during December 2000, setting out control measures regarding the
production, import, export, disposal and use of the twelve most no-
torious POPs. According to this treaty, governments are to promote
the best available technologies and practices for replacing existing
POPs while preventing the development of new ones.
Having negotiated an international ban (and one, unlike the Kyoto
Protocol, which has the support of U.S. President George W. Bush),
the struggle to eliminate POPs cannot yet be retired to a history of
environmental finished business. The Stockholm Convention is a
design for work to be done that will cause fundamental changes in
many industrial processes from the printing of books to the man-
ufacture of Barbie dolls.
Quite without malicious intentions, the chemical industry has
put all of us in its experimental beaker. “We are conducting a vast
toxicologic experiment, and we are using our children as the exper-
imental animals,” said Philip Landrigan, chairman of preventative
medicine at the Mount Sinai School of Medicine (Moyers 2001).
According to Joe Thornton,
It makes no sense to presume that the thousands of organochlorines not

yet tested will somehow turn out to be safe, when virtually every organo-
chlorine investigated to date causes one or more toxic effects. . . . Addressing
organochlorine as a class does not mean an outright ban. Because chlorine
chemistry has invaded every corner of the economy, it would be disastrous
to end production and use of organochlorines overnight. The only practical
approach is a planned process to replace chlorine-based technologies grad-
ually with cleaner alternatives. (Thornton 2000, 353, 355)
Synthetic organochlorines are created by combining the mole-

cules of existing elements (usually, for the chemicals under discus-
sion here, carbon, hydrogen, and chlorine) into combinations not
heretofore present in nature. The manufacture of such chemicals
accelerated during World War II, when, by accident, scientists seek-
ing chemical weapons discovered that their creations killed insects.
By the late 1940s, several insecticides (the most notable, at the time,
being DDT) were introduced to combat insect infestations. The new
chemicals were sprayed liberally on forests, farms, and towns. The
production of synthetic pesticides rose fivefold during the fifteen
years between 1947 and 1962, when Silent Spring was published.
By the middle 1990s, 100,000 synthetic chemicals had been in-
6 The Dirty Dozen
vented, and roughly 1,000 new ones were being introduced each
year (Colborn, Dumanoski, and Myers 1996, 226).
The production of synthetic pesticides, herbicides, and fungicides
for consumption in the United States began in earnest at the end of
World War II and had risen to about 300 million kilograms a year
by 1962, when Rachel Carson published Silent Spring. Production
peaked in 1975 at slightly more than 700 million kilograms a year
and then began a slow decline with the enforcement of environmen-
tal regulations (Pimentel and Lehman 1993, 94).
Synthetic organochlorines have become big business.
At least 11,000 organochlorines are produced commercially. Many thou-

sands more are created as by-products during the manufacture, use and
disposal of these initial 11,000. Only a few of the commercial organochlo-
rines have been tested for carcinogenicity and a few other effects. Fewer still
have been tested for their abilities to disrupt the human endocrine system,
alter the sexual, neurological and immunological development during pre-
and postnatal periods, or any of a long list of equally subtle but potentially
devastating effects. Currently, it takes more than five years and hundreds
of thousands of dollars to gather basic toxicological data for one single com-
pound. (Allsopp, Costner, and Johnston 1995)
Expenditures on pesticides in the United States, in constant 1996

dollars, increased from roughly $3 billion in 1979 to about $10 bil-
lion in 1997 (Berenbaum, 2000, 59). By 1998, the global chemical
pesticide market was $31 billion, a figure that was rising between
1 and 2 percent a year (Berenbaum, 2000, 145). The United States
has no centralized reporting of pesticide expenditures, and so all
figures are estimates. Expenditures appear to be rising roughly 3
percent per year in the United States, indicating a total of perhaps
$11 billion by 2002.
Of all the pollutants released into the environment by human ac-
tivity, POPs are among the most dangerous. They are highly toxic,
causing an array of adverse effects, notably death, disease, and
birth defects, among humans and animals. Specific effects can in-
clude cancer, allergies and hypersensitivity, damage to the central
and peripheral nervous systems, reproductive disorders, and dis-
ruption of the immune system.
POPs have been implicated in the rising incidence of certain
cancers (e.g. breast, prostate) and rising rates of endometriosis, as
well as reproductive disorders such as infertility, declining sperm
Introduction 7
counts, fetal malformations, neurobehavioral impairment, and

immune-system dysfunction.
In Silent Spring, Rachel Carson’s main focus was DDT, which was
invented by a German chemist in 1874. It was not used to kill in-
sects until 1939, however. As an insecticide, DDT was first used on
a large scale during the Naples typhus epidemic of 1943–1944; DDT
was used by the Allied armed forces during the rest of World War II
before the “war” against insects was joined on the home front in
1945.
Certain themes in Silent Spring resonate through the decades,
even though the scientific landscape of environmental toxicology
has changed materially in four decades:
I contend, therefore, that we have allowed these chemicals to be used with

little or no advance investigation of their effects on soil, water, wildlife, and
man himself. Future generations are unlikely to condone our lack of pru-
dent concern for the integrity of the natural world that supports all life.
(Carson 1962a, 13)
In less than two decades of their use, the synthetic pesticides have been so
thoroughly distributed throughout the animate and inanimate world that
they occur virtually everywhere. (Carson 1962a, 15)
[T]he chemist’s ingenuity in devising insecticides has long ago outrun bio-
logical knowledge of the way these poisons affect the living organism [the
human body]. (Carson 1962a, 25)
Agencies concerned with vector-borne disease are at present coping with

their problems by switching from one insecticide to another as resistance
develops. But this cannot go on indefinitely, despite the ingenuity of the
chemists in supplying new materials. . . . [W]e are traveling a one-way street.
No one knows how long that street is. If the dead end is reached before
control of disease-carrying insects is achieved, our situation will indeed be
critical. (Carson 1962a, 271)
Two present-day observers note that the register of potentially

toxic organochlorines has multiplied since the time of Silent Spring:
Today, we can add vastly to Rachel Carson’s list [of problematic chemical
toxins]. Humankind is exposed to thousands of other chemical substances
in ever-increasing quantity and variety. Of the 11 million substances
known, some 60,000 to 70,000 are in regular use. Yet, toxicological data
are only available for a fraction of the more than 3,000-odd chemicals that
account for 90 percent by mass of the total used. The data on the environ-
8 The Dirty Dozen
mental and ecotoxicological properties of such substances are even more

scanty. (Van Emden and Peakall 1996, x)
Carson wrote only a decade and a half after organochlorines be-

came widespread in the world environment. From the development
of DDT grew a chemical industry that was still expanding as Carson
described it in Silent Spring. Four decades later, Carson’s original
list of environmental troublemakers has multiplied several-fold.
Silent Spring contains barely a mention of some chemicals that are
at the top of everyone’s list today, such as dioxins, PCBs, and chlo-
rofluorocarbons (CFCs).
By the middle 1980s, new pesticides were being introduced by
industry much more quickly than science and government could
evaluate them for health hazards. The National Academy of Sci-
ences estimated at that time that only 10 percent had been tested
adequately to permit accurate assessment of health hazards; on 38
percent of pesticides available on the open market, for anyone’s use,
no toxicity information existed (Marco, Hollingsworth, and Durham
1987, 10).
These chemicals resist the natural processes of degradation by
light, reactions with other chemicals, and biological processes. They
are, therefore, potentially toxic for decades or centuries. The body
cannot readily excrete persistent contaminants except through
breast-feeding, and so most of the targeted POPs typically have long
half-lives in the body, and with continued exposure their concen-
trations grow higher over time. Persistent contaminants are now
pervasive in the food web, with animal products, including meat,
fish, and milk, the primary routes of human exposure (World Wild-
life Fund 2000).
No wonder even George W. Bush supports the Stockholm Con-
vention to eliminate the dirty dozen. Evidence described in the
chapters to come indicates just how dangerous these chemicals
have become for the ecosystem of the entire Earth, especially for the
most vulnerable people and animals in the Arctic. For them, POPs
pose a fundamental threat to the survival of future generations.
REFERENCES
Allsopp, Michelle, Pat Costner, and Paul Johnston. 1995. Body of Evidence:
The Effects of Chlorine on Human Health. London: Greenpeace Inter-
national. http://www.greenpeace.org/⬃uk/science/hdc/body.txt.
Introduction 9
Allsopp, Michelle, Ben Erry, Ruth Stringer, Paul Johnston, and David San-
tillo. 2000. “Recipe for Disaster: A Review of Persistent Organic Pol-
lutants in Food.” Greenpeace Research Laboratories and University
of Exeter (U.K.) Department of Biology. March. http://www.green
peace.org/⬃toxics/reports/recipe.html.
Berenbaum, May, ed. Committee on the Future Role of Pesticides in U.S.
Agriculture. Board on Agriculture and Natural Resources and Board
on Environmental Studies and Toxicology. Commission on Life Sci-
ences, National Research Council. The Future Role of Pesticides in
U.S. Agriculture. Washington, D.C.: National Academy Press, 2000.
Carson, Rachel. 1962a. Silent Spring. Boston: Houghton-Mifflin.
Carson, Rachel. 1962b. Silent Spring. Westport, Conn.: Fawcett.
Colborn, T., D. Dumanoski, and J. P. Myers. 1996. Our Stolen Future: Are
We Threatening Our Fertility, Intelligence, and Survival? A Scientific
Detective Story. New York: Penguin.
Cook, Judith, and Chris Kaufman. 1982. Portrait of a Poison: The 2,4,5-T
Story. London: Pluto Press.
Diamond, E. 1963. “The Myth of the ‘Pesticide Menace.’” Saturday Evening
Post, September 21, 17–18.
Marco, Gino J., Robert M. Hollingsworth, and William Durham, eds. 1987.
Silent Spring Revisited. Washington, D.C.: American Chemical
Society.
Moyers, Bill. 2001. “Trade Secrets: A Moyers Report.” Program transcript.
Public Broadcasting Service, March 26. http://www.pbs.org/trade
secrets/transcript.html.
Pimentel, David, and Hugh Lehman, eds. 1993. The Pesticide Question: En-
vironment, Economics, and Ethics. New York: Chapman and Hall.
Thornton, Joe. 2000. Pandora’s Poison: Chlorine, Health, and a New Envi-
ronmental Strategy. Cambridge, Mass.: MIT Press.
Van Emden, Helmut F., and David B. Peakall. 1996. Beyond Silent Spring:
Integrated Pest Management and Chemical Safety. London: Chapman
and Hall and United Nations Educational Program.
Waddell, Craig, ed. 2000. And No Birds Sing: Rhetorical Analysis of Rachel
Carson’s “Silent Spring.” Carbondale: Southern Illinois University
Press.
Whitten, J. L. 1966. That We May Live. Princeton, N.J.: D. Van Nostrand.
World Wildlife Fund. 2000. “Toxics—What’s New.” http://www.worldwild
life.org/toxics/progareas/pop/pop_rep.htm.
1
Persistent Organic Pollutants: The Basics
Commercial organochlorines have become pervasive in our every-

day lives. They are as close at hand as the pesticides many people
use on their lawns and gardens, the solvents auto mechanics use
in their shops, and the plastics we use to store our foods. Organo-
chlorines (organo refers here to the presence of carbon in combi-
nation with chlorine) are part of many lubricants and refrigerants.
They are used in soaps, shampoos, deodorants, and cosmetics, as
well as toothpastes and mouth rinses. Many children’s toys, includ-
ing the ubiquitous Barbie doll, are made of flexible polyvinyl chlo-
ride (PVC) (Allsopp, Costner, and Johnston 1995).
The “Dirty Dozen” of this book’s title refer to the twelve chemicals
that have been short-listed for elimination by international protocol.
They include organochlorine pesticides (DDT, chlordane, mirex,
hexachlorobenzene, endrin, aldrin, toxaphene, heptachlor) and in-
dustrial chemicals including PCBs, as well as the super-toxic di-
oxins and furans.
Persistent organic pollutants (POPs) are chlorine-based chemical
compounds and mixtures that share four characteristics: high tox-
icity, persistence, a special affinity for fat, and a propensity to evap-
orate and travel long distances. Most people might be surprised to
learn how common these toxic compounds are in their daily lives.
Incinerators of all types emit dioxins, furans, and PCBs. Several
times in Europe during the 1990s, emissions from municipal-waste
or hazardous-waste incinerators have deposited these toxins on
nearby grazing land, leading to contamination of milk. Persistent
contaminants typical of industrial regions such as the Great Lakes
have been found in albatrosses on remote Midway Island in the
12 The Dirty Dozen
middle of the Pacific. Penguins in Antarctica have been found to be

contaminated with a breakdown product of the pesticide chlordane
and other persistent chemicals.
Each of these synthetic chemicals is built on a chlorine base.
Assessing the potential of any given chemical, either in the human body or
in the environment, one question is of overriding importance: does it contain
chlorine? Chlorine is highly reactive—that is, it combines very readily with
certain other elements and it tends to bind to them very tightly. . . . Chlo-
rine’s ability to snap firmly into place, and to anchor all sorts of chemical
structures, has made it, in the words of W. Joseph Stearns, director of chlo-
rine issues for the Dow Chemical Company, “the single most important in-
gredient in modern [industrial] chemistry.” (McGinn 2000, 33)
Heat-resistant PCBs became standard liquid insulation in elec-

trical transformers, which are widely used in all electrical grids.
Roughly 70 percent of all PCBs ever manufactured are still in use
or in the environment, often in landfills, where they gradually seep
into water tables (McGinn 2000, 34). Reclamation of copper from
cables causes the release of dioxins, furans, and PCBs (from the
burning of the PVC plastic coatings on the cables). In southern Tai-
wan, fish from aquaculture ponds have been found to be highly con-
taminated from the nearby burning of electrical cables and credit
cards. Two accidental polyvinyl chloride fires in Germany in 1992
and 1996 also caused local contamination by dioxins and furans.
For a time, the sale of several food products was banned in Ger-
many. The use of chemical pesticides has been a central part of the
“Green revolution,” which aims to increase crop yields in Asia.
Brominated flame retardants, designed to reduce the fire hazard
in personal computers and other electrical consumer products,
have been found in whales living in the deep oceans. Synthetic
musk compounds, used as fragrances in detergents, fabric soften-
ers, and other household products, have been found in human
breast milk. TributylTin (TBT), an additive in ship paint, is held re-
sponsible for the development of male sex characteristics in female
snails. TBT is detectable in fish, mussels, and other marine life,
particularly in harbors and coastal waters.
“These examples may just be the tip of the iceberg,” said Paul
Johnston, head of Greenpeace’s research laboratories. “For sub-
stances which have been banned for some time, levels in wildlife are
decreasing only slowly. At the same time, many chemicals with sim-
Persistent Organic Pollutants 13
ilarly hazardous properties continue to be used and released to the

environment every day” (POPs Invade 1999).
Since 1945, annual global production of pesticides has increased
twenty-seven-fold, from 0.1 million tons to 2.7 million tons (McGinn
2000, 32). In addition, pesticide formulations that are sold to the
public have become more potent; current pesticide formulations of-
ten are ten to a hundred times as toxic as they were in 1975 (McGinn
2000, 32). About 11,000 organochlorines are in production. The
most common plastic is now polyvinyl chloride (PVC). Global pro-
duction of PVC rose more than 70 percent, from 12.8 million tons
to 22 million tons, between 1988 and 1996 (McGinn 2000, 32).
Many new chemical products have been brought to market to in-
crease human comfort and convenience (and corporate profits),
with little forethought to their eventual impacts (two of which are
carcinogenesis and the destruction of stratospheric ozone) on the
natural world and its inhabitants. The number of chemicals regis-
tered with the U.S. Environmental Protection Agency (EPA) for com-
mercial use reached 80,000 during 2000; roughly 3,800 of these
are regarded by the agency as high-production-volume chemicals.
Fewer than half these chemicals have been tested for toxicity to hu-
mans. Only 8 to 10 percent have been tested specifically for their
effects on the developing brain, the developing immune system, the
developing reproductive organs, or the endocrine system of babies
(Moyers 2001). Tens of thousands of chemicals reached the market
before testing was required.
The United Nations Environmental Program’s Governing Council
in 1995 identified twelve persistent organic pollutants as subjects
of an eventual ban on manufacture and use worldwide because they
damage the ecosphere and the diversity of life supported by it. While
many of these pollutants had been banned in the United States,
other countries continued to manufacture and use them until they
were outlawed by international protocol in late 2000. The interna-
tional ban of the dirty dozen (see the following list) was negotiated
in Stockholm late in 2000; ratification of the protocol had been
largely completed as this book was being prepared for publication.
The Dirty Dozen

Aldrin
Uses/Production: Control termites and protect corn, potatoes, and cotton
from insects
Treaty Action: Elimination
14 The Dirty Dozen
Chlordane
Uses/Production: Protect agricultural crops and control termites
DDT
Uses/Production: Protect agricultural crops and kill insects that carry
malaria and typhus
Treaty Action: Elimination; exemptions for disease control
Dieldrin
Uses/Production: Control termites, soil insects, and insects carrying
disease
Dioxins and furans
Uses/Production: By-products from waste incineration and industry
Treaty Action: Reduction and minimization
Endrin
Uses/Production: Protect cotton and grains from insects, rodents, and
birds
Heptachlor
Uses/Production: Control termites, soil insects, and insects carrying
malaria
Hexachlorobenzene
Uses/Production: Protect wheat from pests; also a by-product of some
chemical manufacture
Mirex
Uses/Production: Control fire ants, leafcutter ants, and termites; fire re-
tardant in plastics
Polychlorinated biphenyls (PCBs)
Uses/Production: Several industrial uses, mainly as electrical insulators
Treaty Action: No new production; reduced use
Toxaphene
Uses/Production: Protect agricultural crops and kill ticks and mites on
livestock
Several of these synthetic chemicals (including PCBs and dioxins,

the best known) actually refer not to single chemicals, but to fami-
lies of chlorine-based compounds. For example, the term dioxin, as
used by toxicologists, refers to a number of substances that share
certain molecular features. They contain chlorine atoms attached
to carbon atoms that are linked to each other in structures known
as aromatic rings. Polychlorinated biphenyls, for example—the
notorious PCBs—often are considered dioxins in discussions of
toxicity.
Many of the dirty dozen were first formulated to kill insects. Al-
drin, one of the dirty dozen, is a pesticide used to control soil insects
such as termites, corn rootworm, wireworms, weevils, and grass-
hoppers. It has been widely used to protect crops such as corn and
potatoes and has been effective in protecting wooden structures
from termites. Like many organochlorines, Aldrin is very toxic to
human beings and other animals. A lethal dose of aldrin for an adult
man (about five grams), provokes muscle twitchings, myoclonic
jerks, and convulsions.
THE PERSISTENCE AND MOBILITY OF POPS

Once a persistent contaminant has evaporated, it can travel thou-
sands of miles in air masses, often hitchhiking on particles (such
as dust) in the atmosphere. Through a process known as the “grass-
hopper effect,” persistent chemicals jump around, evaporating in
warm conditions and then settling in cool spots. When the tem-
perature is right, POPs will again take flight and continue their hop-
scotching travels. Scientists have detected POPs everywhere on
Earth they have looked for them, even in regions where these syn-
thetic chemicals have never been used. For example, Eric Dewailly
first visited the Canadian Arctic to establish a baseline for contam-
ination in urban areas of Quebec. He quickly found POPs there at
levels that were higher than those in Canadian cities (Dewailly et al.
1993, 173–76).
16 The Dirty Dozen
The pollution of PCBs (among other organochlorines) is truly

global. They have been measured in ocean-water samples from the
Sargasso Sea, the North Sea, the western North Pacific, the South
Pacific, the Indian Ocean, and the seas around Antarctica, among
other places thousands of miles from their emission sources (Thorn-
ton 2000, 34). Most POPs (most notably PCBs and dioxins) diffuse
easily throughout the ecosphere. Many of these pollutants also flow
(via ocean and air currents) to “cold sinks,” such as the Arctic, the
Antarctic, and higher elevations of mountain ranges.
The persistence of organochlorine POPs varies considerably; some
have half-lives of less than a year, but others’ decay rates are mea-
sured in millions (and even billions) of years. Hexachloroethane, for
example, has a half-life in pure water of 1.8 billion years, and 1,2-
dichloroethylene’s half-life is estimated at 21 billion years (Thornton
2000, 33).
Since POPs are soluble in fats (in technical terms, they are lipo-
philic), the highest levels are usually found in fatty foods such as
meat, fish, and dairy products. POPs can be detected, however, at
lower concentrations in vegetables, fruits, and cereals. Many POPs
reach their human hosts through foods that have been liberally
doused with these compounds on their way to the table, usually to
minimize insect damage. Farm workers who harvest these foods
sometimes have been exposed at unhealthy levels. Food-borne per-
sistent organochlorines are readily absorbed into the human body.
By the late 1980s, 300,000 farm-worker poisonings a year were be-
ing reported in the United States, and the United Farm Workers
were making a major issue of banning the most dangerous herbi-
cides and pesticides.
Direct application of organochlorine pesticides leads to residues
on crops. Contamination of the human food chain has also occurred
when contaminated wastes have been mixed with livestock feed-
stuffs or directly with food intended for human consumption.
Once they have been absorbed, these unnatural chemicals evade
the body’s defenses. They cannot be shed using the body’s pro-
cesses for detoxifying and excreting other wastes that could become
toxic. Instead, they accumulate in body fat, from which they are
released most rapidly during periods when fat stores are drawn
down, such as periods of hunger (including aggressive dieting) and
lactation associated with pregnancy.
Throughout a woman’s lifetime, the store of persistent contami-
nants increases in her body fat. By unfortunate coincidence, the
demands of pregnancy and breast feeding draw down these fat re-
serves, and so a load of contaminants a mother has taken decades
to accumulate passes to her baby in a very short time. Even worse,
these hormone-disrupting contaminants hit the baby at the most
vulnerable period of human development. The same goes for most
other mammals.
For these reasons, and others, children who are breast-fed in cold
sink areas, such as in the Arctic among the Inuit, are at particular
risk. (The fact that the Inuit diet centers on animals, such as polar
bears and seals, which also are accumulating these chemicals in
their body fat, adds to the danger.)
DISSENTERS TO THE MAJORITY PARADIGM

The behavior of organochlorines in the atmosphere and oceans
was largely unknown to human science before 1985. Despite the
recent arrival of a new scientific paradigm on the issue, a minority
of scientists disagree, as with climate change. For example, Ames,
Profet, and Gold (1990) have made a case that animals, including
humans, employ natural defenses against synthetic chemicals such
as dioxins. Comparing indole carbinol (found in broccoli) and alco-
hol with dioxin, Ames, Profet, and Gold conclude that “animals have
a broad array of . . . defenses to combat the changing array of toxic
chemicals in plant food (nature’s pesticides) . . . [T]hese defenses
are effective against both natural and synthetic toxins.”
These researchers argue that the human body is “well-buffered”
against toxins because much of its cellular material is quickly re-
placed, some of it within a few days. DNA also repairs itself, they
argue. They also believe that “Plant antioxidants do not distinguish
whether carcinogens are synthetic or natural in origin.” While syn-
ergism between synthetic chemicals can multiply their toxicity,
“This is also true of natural chemicals, which are by far the major
source of chemicals in the diet.” Similarly, this school of thought
maintains that fat-soluble natural toxins “bioconcentrate” as effec-
tively as their artificial cousins. A cooked steak contains hydrocar-
bons that mimic dioxin, they contend.
BIOACCUMULATION
The key to the potency (and toxicity) of POPs is bioaccumulation
(also sometimes called biomagnification). While studying Great
18 The Dirty Dozen
Lakes wildlife, Theo Colborn found that microscopic organisms pick

up persistent pollutants in sediments. They, in turn, are consumed
by zooplankton, which are consumed by mysids (small, shrimp-like
creatures). A smelt may eat the mysids, and a lake trout may eat
the smelt. By the time a herring gull (or a human being) eats the
lake trout, its body may contain 25 million times the concentration
of the pollutant found in a lake’s sediment.
Another key to the potency of POPs is the tiny amount required
to induce toxicity. Effects can be identified in doses measured in
parts per billion—the equivalent, according to Colborn, et al., 1996)
of a cocktail made from a few drops of gin and the tonic contained
in a six-mile long train of railroad tank cars (Colborn, Dumanoski,
and Myers 1996, 40). A single exposure of laboratory animals to
some forms of dioxin (ranging from a dose of less than one micro-
gram to a few milligrams per kilogram of body weight) is usually
lethal (Lok and Powell 2000). Only short-term prenatal exposure of
the mother to dioxins is required to produce long-term developmen-
tal and immunological problems in offspring during its entire life-
span (Lok and Powell 2000).
Even minute levels of PCBs, sometimes less than five parts per
billion, may provoke biological damage over long periods of time.
Monkeys fed a PCB level typical of concentrations found in human
breast milk showed “significantly impaired learning and perfor-
mance skills when tested at three years of age” (Schettler et al.1999,
177). The monkeys’ blood levels of PCB, at two to three parts per
billion, were similar to typical levels in general human populations
(Rice and Hayward 1997).
“The science is showing that extremely small amounts of dioxin
delivered at critical times are enough to permanently disrupt fetal
development and lead to very serious repercussions,” said Frederick
vom Saal, an expert on environmental chemicals at the University
of Missouri at Columbia. “Today you don’t find anybody saying
small amounts of dioxin are likely to be safe,” vom Saal said. “It’s
not a position that any responsible person is taking” (Allen 1997a).
CONTAMINATION OF FOOD
A report issued by the Pesticide Action Network North America
and Commonweal documents widespread contamination of U.S.
food with many POPs that have been banned in the United States
for many years. The report asserted that an average American may
experience as many as seventy exposures a day to POPs, most of
them in food. The report, “Nowhere to Hide: Persistent Toxic Chem-
icals in the U.S. Food Supply,” analyzes chemical residue data col-
lected by the Food and Drug Administration (FDA) and finds POPs
in all food groups, from baked goods and meats to fresh fruits and
vegetables (Schafer 2000).
These residues cannot be washed off produce with water. Accord-
ing to the report,
Virtually all food products are contaminated with POPs . . . including baked
goods, fruit, vegetables, meat, poultry and dairy products. It is not unusual
for daily diets to contain food items contaminated with three to seven POPs.
A typical holiday dinner menu of 11 food items can deliver thirty-eight “hits”
of exposure to POPs, where a “hit” is one persistent toxic chemical on one
food item. . . . The top 10 POPs-contaminated food items, in alphabetical
order, are: butter, cantaloupe, cucumbers (pickles), meatloaf, peanuts, pop-
corn, radishes, spinach, summer squash, and winter squash. (Schafer
2000)
A Greenpeace report published in March 2000 warned that much

of the world’s food is contaminated with POPs. The report, “Recipe
for Disaster,” reviewed existing data on food worldwide and revealed
that some foodstuffs, particularly fish, meat, and dairy products,
contain levels of POPs that exceed internationally agreed-upon lim-
its (Allsopp et al. 2000). “Our food chain is the main route of human
exposure to these highly toxic chemicals. The widespread contam-
ination of food with manufactured chemicals in both industrialized
and less-industrialized countries is fundamentally unacceptable,”
said David Santillo of the Greenpeace International Science Unit
(Santillo 2000). “In many cases, we are being exposed to levels in
excess of the maximum intakes deemed tolerable by international
bodies,” he added (Cooper 2000). Some POPs are produced inten-
tionally, such as the pesticide DDT, which was first synthesized in
Germany during 1874 but remained a laboratory curiosity until its
pesticidal properties were discovered in 1939.
Allsopp and colleagues (2000) found that tolerable daily intakes
for toxic POPs in food, as set by the World Health Organization
(WHO), were exceeded in Spain, India, and parts of Canada as well
as in sections of southern Sweden and southern Taiwan, where
many people eat a large amount of fish. David Santillo also indicated
that “Consumption of fish-oil dietary supplements may lead to ex-
20 The Dirty Dozen
cessive intake of dioxins in U[nited] K[ingdom] children” (Santillo

2000). The same report found that fish in Spain and Australia con-
tained particularly high levels of certain POPs in excess of maximum
levels set by the WHO. Meats in Vietnam and Mexico and dairy prod-
ucts in Hong Kong, Argentina, and Mexico were found to be similarly
afflicted.
The same report (Santillo 2000) described instances in which food
has been contaminated from local pollution sources, such as incin-
erators or metal recycling centers, as well as from the mixing of
waste with animal feed, such as PCB-contaminated oils (as was the
case during the 1999 dioxin chicken scandal in Belgium, which is
described below). The report asserts that the scale and scope of POP
pollution is not yet known, because there are large gaps in the sci-
entific data on levels of POPs in food. Most studies are restricted to
investigating a limited range of organochlorines, such as DDT and
PCBs, while many other POPs remain unexamined. “Given that
POPs are a global problem, it is likely that today’s findings are just
a glimpse at a much more widespread problem. Unless action is
taken now to phase out the production and use of POPs, and the
processes which generate them, our food and environment will re-
main contaminated for generations to come” (Santillo 2000).
Organochlorine levels in fish from the Great Lakes are still high,
although levels have generally declined in recent years. DDT levels
in meat have fallen in Australia and Canada. There have been some
regional declines in PCBs in marine fish. DDT levels have generally
decreased in marine fish but levels in areas of the tropics indicate
continued input to the marine environment. In human milk, con-
centrations of dioxins and furans have not increased in Western
countries in recent years, and levels in some European countries
have declined. A decreasing trend has been observed for DDT in
Europe, where it is banned, but not in Mexico, where it is still used.
Levels of PCBs and chlordane in human milk do not appear to have
declined in countries where levels have been monitored. These ex-
amples indicate that although levels of some compounds have de-
clined, others remain stable because of their persistence and
because contamination of the environment has continued.
Within the past few years, high levels of DDT have been detected
in meat from Thailand, Vietnam, and Mexico. For dioxins and fu-
rans, veal is the most highly contaminated meat because of the high
proportion of milk in calves’ diets. In India, a high proportion of

tested milk samples were found to be highly contaminated with
DDT; some exceeded national limits. High levels of DDT were ap-
parent in milk in Hong Kong and Argentina. Residues of aldrin and
dieldrin were also reported to be high in milk from these countries,
and levels of heptachlor and heptachlor epoxide exceeded safety
standards in Hong Kong, Argentina, and Mexico.
DDT residues have been found in tea and coffee. A 1994 study
reported that levels in vegetables from Australia gave evidence of
recent application on crops despite a ban on using DDT there.
Wheat stored in gunny sacks in India was found to be contaminated
with DDT.
Sports anglers catching fish along the north shore of the Gulf of
the St. Lawrence River and individuals eating fish from the Great
Lakes carry notably high body burdens of organochlorines, includ-
ing PCBs and dioxins (Dewailly et al. 1994; Fein et al. 1984). Ele-
vated concentrations of dioxins and related organochlorines also
have been documented in milk produced near municipal and in-
dustrial waste incinerators, as well as near other industries (Lassek,
Jahr, and Mayer 1993; Liem et al. 1991).
In an attempt to protect public health, regulatory agencies have
set permissible levels in specific foods, maximum residue limits,
that should not be exceeded. For levels of organochlorines in diet,
the Food and Agricultural Organization (FAO) and the WHO have
set levels that are deemed to be “safe,” called tolerable daily intakes
(TDIs) or acceptable daily intakes (ADI). These regulatory limits are
set using toxicity data from studies in laboratory animals and some
data from human studies.
Risk assessments used to determine the ADIs/TDIs is a process
that is fraught with uncertainties. Furthermore, results of toxicity
testing in animals may be inappropriate for detecting certain health
effects, potentially leaving health effects undetected. Risk assess-
ment assumes a threshold dose of a chemical below which there are
no health effects, a dose at which acceptable levels of exposure may
be set. However, for some POPs, there may be no such threshold
dose. Another complicating factor: Usually people are exposed to
mixtures of chemicals. Sometimes two or more chemicals have ef-
fects in synthesis only. Therefore, it is unlikely that limits estab-
lished for singular organochlorines in diet are truly protective of
human health in the real world of multiple exposures.
22 The Dirty Dozen
A BRIEF HISTORY OF POPS

During 1774 Swedish pharmacist Carl Wilhelm Scheele released
a few drops of hydrochloric acid onto a piece of manganese dioxide.
Within seconds, a greenish-yellow gas arose, marking the first sci-
entific observation, quite by accident, of chlorine. At first, observers
thought the gas was a compound of oxygen. Not until the nineteenth
century did the English chemist Sir Humphrey Davy recognize chlo-
rine as a chemical element. Davy gave the element its name after
the Greek word khloros, anglicized to “chloric gas” or “chlorine,”
which became the seventeenth element on the periodic table.
By midcentury, scientists and manufacturers came to under-
stand chlorine’s powerful disinfectant qualities, which stem from
its ability to bond with and destroy the outer surfaces of bacteria
and viruses. Chlorine was first used as a disinfectant during 1846
to prevent the spread of child-bed fever in the maternity wards of
Vienna General Hospital in Austria. Later, during the same century,
chemists began to experiment with compounds of chlorine as they
learned that it has an extraordinary ability to extend a chemical
“bridge” between various elements and compounds that would not
otherwise react with each other. By the late 1920s and 1930s, syn-
thetic organic compounds were being invented and marketed with
no evident concern for environmental effects.
The first synthetic organochlorines were created by accident dur-
ing the late eighteenth century as by-products of the synthesis and
use of elemental chlorine. At about the same time, Charles Darwin’s
interest in evolution led him to conduct a number of experiments
dealing with plant reproduction. During these investigations, Dar-
win discovered that plant growth and reproduction are controlled
by hormones that deliver chemical “signals” throughout any given
plant. Auxin was isolated during 1928, followed by research aimed
at using these chemicals to increase crop yields by speeding up the
growth of plants.
PCBs are a combination of chlorine atoms with a molecule con-
taining two joined hexagonal benzene rings, known as a biphenyl.
Before they were detected throughout the environment, and before
their toxic effects were known, PCBs were deemed a wonder chem-
ical useful in just about any application in which fire suppression
is an advantage, notably in the transmission of high-voltage elec-
tricity. Various PCBs were used to impart inflammability to wood
and plastics, to preserve and protect rubber, and to water-seal
stucco. They found many uses in varnishes, inks, and paints, as

well as pesticides. About 1970, PCBs were used to create “carbon-
less” carbon paper.
By the mid-1930s, workers and some customers at Halowax Cor-
poration (later part of Union Carbide) and General Electric (GE) were
suffering outbreaks of chloracne—“small pimples with dark pig-
mentation of the exposed area, followed by blackheads and pus-
tules” (Montague 1993). During 1936 three workers at Halowax
Corporation died. The company hired Harvard University research-
ers to determine a cause. The researchers tested the air in several
Halowax manufacturing plants and then designed experiments to
replicate these levels and expose experimental rats to them. They
reported that
The chlorinated diphenyl is certainly capable of doing harm in very low con-
centrations and is probably the most dangerous [of the chlorinated hydro-
carbons studied]. . . . These experiments leave no doubt as to the possibility
of systemic effects from the chlorinated naphthalenes and chlorinated di-
phenyls. (Drinker et al. 1937, 283)
The Swan Chemical Corp. (later a division of Monsanto) had be-

gun manufacturing PCBs in commercial quantities during 1929.
Eight years later, following the aforementioned experiments, the
Harvard School of Public Health hosted a one-day meeting on sys-
temic effects of certain chlorinated hydrocarbons including “chlo-
rinated diphenyl” (an early name for PCBs). The meeting was
attended by representatives from Monsanto, GE, the U.S. Public
Health Service, and the Halowax Corporation, among others (Mon-
tague 1993). At this meeting F. R. Kaimer, an assistant manager of
GE’s Wireworks at York, Pennsylvania, said that one GE factory
had in the neighborhood of 50 to 60 men afflicted with various degrees of

this acne about which you all know. Eight or ten of them were very severely
afflicted—horrible specimens as far as their skin conditions was concerned.
One man died and the diagnosis may have attributed his death to Halowax
vapors, but we are not sure of that. (Drinker et al. 1937, 283)
As early as the 1930s, tests of laboratory animals revealed estro-

genic properties in several synthetic organochlorines. Organochlo-
rine estrogen mimicry by DDT was reported in chickens as early as
1950 (Dodds and Lawson 1938; Dodds, Goldberg, and Lawson
1938; Dodds et al. 1938). The Danish chemist Søren Jensen was
the first, during the middle 1960s, to detect residues of PCBs
24 The Dirty Dozen
throughout the environment; he found it even in hair samples taken

from his wife and daughter. By the middle 1990s, a battery of tests
costing about $2,000 could reveal to anyone the presence, in his or
her body, of roughly 250 chemical contaminants, most of them in
trace amounts. The tests could be carried out on anyone, anyplace
on Earth, with similar results (Colborn, Dumanoski, and Myers
1996, 106).
Coincident with the introduction of DDT into the world ecosys-
tem, the first warning sign appeared that some manufactured
chemicals might spell serious trouble. In 1944 scientists found res-
idues of DDT in human fat. Seven years later, another study
brought disturbing news of DDT contamination in the milk of nurs-
ing mothers. During the early 1950s, naturalists observed thinning
eggshells and rapidly declining populations of bald eagles and other
birds. In 1962 Rachel Carson documented the growing burden of
contamination in Silent Spring, which detailed the devastating im-
pact of persistent pesticides on wildlife and warned about hazards
to human health.
Even as environmental alarm bells began to ring, the use of syn-
thetic chemical pesticides grew swiftly throughout the 1960s and
1970s. Japan experienced a thirty-three-fold increase in pesticide
use between 1950 and 1974; little increase in the agricultural yield
was associated with this lavish use of pesticides. Between 1945 and
the late 1970s, pesticide use rose tenfold in the United States, while
crop losses to pests doubled (Van Emden and Peakall, 1996, 65).
In the meantime, by 1969, research indicated that dioxins in
2,4,5-T cause birth defects in mice. By this time, cooking oil was
found to have been contaminated by PCBs. The “Yusho” incident
occurred in Japan in 1968 and the “Yu-Cheng” incident occurred
in Taiwan in 1979, both affecting around 2,000 people. Increased
mortality rates were recorded following the incidents, and a broad
spectrum of adverse health effects were reported. Children exposed
in utero were most severely affected.
Within a century and a half, according to the Chlorine Chemistry
Council (CCC), “The chlorine industry [was] support[ing] nearly 2
million jobs with an annual payroll of more than $52 billion” in the
United States alone. “In fact,” asserted the CCC, “Almost 40 percent
of U.S. jobs and income are in some way dependent on chlorine”
(Chlorine Chemistry Council 2001). Furthermore, asserted the
CCC, “Chlorine is irreplaceable in our economy. A ban on chlorine’s
use would cost U.S. consumers more than $90 billion per year for
alternative products and process—with no guarantee of equivalent
performance or quality” (Chlorine Chemistry Council 2001). By the
year 2000, approximately 12 million tons of chlorine were being pro-
duced in North America.
According to the CCC, the largest volume of chlorine, about 35
percent, is used in the production of other chemicals, including
many pharmaceuticals. Plastics consume more than 25 percent of
the yearly output. A significant amount of chlorine, around 18 per-
cent, is used to produce solvents for metalworking, dry cleaning,
and electronics. Roughly 10 percent is used for pulp and paper
bleaching. Chlorine is also used in drinking-water purification, as
well as wastewater and swimming-pool disinfection (Chlorine
Chemistry Council 2001).
AGENT ORANGE IN VIETNAM

At the time of the first Earth Day, in the spring of 1970, the United
States was pouring dioxin (as an active ingredient of Agent Orange)
on the jungles of Vietnam, Laos, and Cambodia in an attempt to
defoliate the jungles and deny insurgents places to hide from aerial
bombing. The guerrillas were said to be “fish” in a “sea” of rural
peoples that would be stripped bare by defoliants. Between 1962
and 1971, at least 12 percent of southern Vietnam’s land area was
doused liberally with nearly 18 million gallons of 2,3,7,8-tetra-
chlorodibenzo-p-dioxin (TCDD), the most potent of dioxin’s many
varieties (Schecter et al. 2001, 435).
U.S. armed forces dropped more bombs (measured by weight) on
Vietnam than it dropped in the entire Pacific Theater during World
War II. By 1971, more than 600 pounds of bombs per person had
been rained on Vietnam. Between 12 percent (U.S. figure) and 43
percent (National Liberation Front figure) of South Vietnam’s land
area was sprayed at least once with defoliants, usually Agent
Orange (Johansen 1972, 4).
Eighteen million gallons of Agent Orange was sprayed over vast
tracts of Southeast Asian forests between 1962 and 1971 in con-
centrations up to 1,000 times as potent as dioxin-based herbicides
sold over the counter in the United States (McGinn 2000, 26).
Large areas of the countryside became unfit for human habitation
during the war, and for several years thereafter. The population of
26 The Dirty Dozen
Saigon, now Ho Chi Minh City, increased tenfold between 1954

(when the war began with French intervention) and 1970, from
300,000 to 3 million people (Johansen 1972, 4).
Most of the herbicides, including Agent Orange, were applied to
populated areas without prior hazard testing. Agent Orange was
applied in large amounts, often haphazardly, by troops taking part
in “Operation Ranch Hand,” whose participants proclaimed that
“Only we can prevent forests,” a play on Smokey the Bear’s slogan,
“Only you can prevent forest fires” (Johansen 1972, 4). Samples
collected in 1970 and 1973 documented elevated levels of TCDD in
milk samples, as well as in fish and shrimp. Nursing mothers who
had been heavy consumers of fish were found to have the highest
levels in their blood (Schecter et al., 2001, 435).
Soon after spraying of Agent Orange and other herbicides began
during the late 1960s, reports increased of deformed births in un-
usually large numbers. Areas sprayed with Agent Orange later re-
ported very high incidences of certain birth defects: anencephaly
(absence of all or parts of the brain), spina bifida (a malformed ver-
tebral column), and hydrocephaly (swelling of the skull).
The Saigon newspaper Tin Sang published descriptions of “mon-
ster babies” born to mothers in areas that had been sprayed. The
newspaper reported that one woman “reported that her newly preg-
nant daughter was caught in a chemical strike, and fainted, with
blood coming out her mouth and nostrils, and later from her vulva.
She was taken to a hospital where she was later delivered of a de-
formed fetus” (Johansen 1972, 4). The same day (October 26, 1969),
Dong Nai, another Saigon newspaper, published a photograph of a
still-born fetus with a duck-like face and an abnormally twisted
stomach. A day later, the newspaper reported that a woman in the
Tan An district who had been soaked with Agent Orange had given
birth to a baby with two heads, three arms, and twenty fingers (Jo-
hansen 1972, 4). Many other similar accounts were published be-
fore the South Vietnamese government shut down the newspapers
for “interfering with the war effort” (Johansen 1972, 4). The South
Vietnam health ministry also began to classify accounts of deformed
births as state secrets.
When these accounts were presented to U.S. Department of De-
fense officials, they were, at first, dismissed as unconfirmed enemy
propaganda. When the accounts persisted and began to be more
specific and numerous, the U.S. armed forces finally stopped using
Agent Orange. The U.S. Air Force later found a “significant and po-
tentially meaningful” relationship between diabetes and blood-
stream levels of dioxins in its ongoing study of people who worked
with the defoliant Agent Orange during the Vietnam War (Brown
2000, A-14; Institute of Medicine 1994). Members of the U.S. armed
services who were exposed to high levels of dioxins were found to be
more prone to development of diabetes than those with low levels of
exposure. People with the highest exposure levels developed dia-
betes most rapidly. While it once dismissed reports of cancers
caused by Agent Orange as groundless, three decades later the U.S.
Army was giving a special medallion—the Order of the Silver Rose—
to soldiers who had been afflicted.
By mid-2001, the U.S. Department of Veterans Affairs was solic-
iting applications for compensation from Vietnam veterans with any
of a large number of “presumptive disabilities”: chloracne, Hodg-
kin’s disease, multiple myeloma, non-Hodgkin’s lymphoma, soft-
tissue sarcoma, acute and subacute peripheral neuropathy, and
prostate cancer (“Bulletin Board” 2001). The same request for
claims asserted that diabetes mellitus soon would be included in its
list of dioxin-induced pathologies.
At roughly the same time, a panel advising the EPA, well-stocked
with industry representatives, was still arguing whether dioxin is
carcinogenic in human beings. After ten years of work, during the
summer of 2000, the EPA released a 3,000-plus page Draft Dioxin
Reassessment, which concluded that “TCDD (and possibly other
closely related structural analogs, such as the chlorinated diden-
zofurans) are carcinogenic to humans and can cause immune-
system alterations; reproductive, developmental, and nervous
system effects; endocrine disruption, altered lipid metabolism; liver
damage; and skin lesions” (Schecter et al. 2001, 436). The EPA
study confirmed many other studies that had linked TCDD and
other forms of dioxin to “cancer and cancer mortality at relatively
high levels in chemical workers and in toxicity studies” (Becher,
Steindorf, and Flesch-Janys 1998; Fingerhut et al. 1991; Flesch-
Janys et al. 1995; Flesch-Janys et al. 1998; National Toxicology Pro-
gram 1998).
An Air Force study, conducted between 1982 and 2000, followed
about 1,000 people who serviced or flew aircraft carrying Agent Or-
ange. Their health was compared to a similar number who also
served in Vietnam but had no known defoliant exposure. “The data
28 The Dirty Dozen
do not prove dioxin causes diabetes, only that there appears to be

a correlation between its level in the blood and the disease. There
could be non-causal reasons for the association” (Brown 2000,
A-14). People with diabetes may have higher levels of dioxins in their
blood because their bodies get rid of the chemical more slowly than
most, for example.
Men who sprayed Agent Orange in Vietnam between 1962 and
1971 were followed to determine whether exposure to dioxin af-
fected their children. Nervous-system disorders were found to be
widespread. Spontaneous abortions, birth defects, and develop-
mental delays also were noted—paradoxically, men who received
low doses of dioxin tended to give birth to more children with these
problems than those who had been exposed at higher levels (Wolfe,
Micalek, and Miner 1995).
Dioxin levels remained very high during the year 2000 in some
areas of Vietnam that had been sprayed with Agent Orange more
than three decades earlier (Schecter et al. 1992). Tests of people in
the city of Bien Hoa (population 390,000), about twenty miles north
of Ho Chi Minh City (formerly Saigon), in particular, evidenced di-
oxin readings 135 times higher than levels in Hanoi, which was not
sprayed. Levels in Hanoi were measured at 2 to 3 parts per billion
of TCDD (roughly background level in today’s world), while blood
levels of 271 p.p.b. were found in the blood of people living in Bien
Hoa (Schecter et al. 2001, 435).
Bien Hoa was used during the war as a major U.S. military base
and chemical depot where dioxin was transported, some of which
leaked into the neighboring Bien Hung Lake, which is connected to
the nearby Dong Nai River. This aquatic system became the conduit
for the spread of dioxin toxicity among many people in the area. The
highest readings were obtained from people who lived near the lake
and had eaten fish from it regularly.
High levels of dioxin were reported not only in people who had
lived in the area during the war, but also in people who had moved
to Bien Hoa from uncontaminated areas many years after the war
ended, illustrating the persistence of dioxin contamination. High
levels also were reported in the bodies of people born in the area
many years after the war ended and the chemical stores (but not
toxic residues) were removed. Even the U.S. Department of Defense
admitted that at least one underground storage tank had ruptured
before 1971, spilling between 5,000 and 7,000 gallons of Agent Or-
ange into the local groundwater. The liberated dioxins thereby fil-
tered into the water table and moved to the lake and the river,
attaching themselves to plants and animals along the way.
The research of Arnold O. Schecter (an environmental scientist at
the University of Texas School of Public Health) and colleagues
clearly indicated how residents of Bien Hoa—some of whom had not
been born during the war—continued to acquire contamination.
The dioxin first dumped in the area by U.S. armed forces was bio-
accumulating up the food chain, from phytoplankton to zooplank-
ton, and then to fish consumed by people:
Persons new to this region and children born after Agent Orange spraying
ended also had elevated TCDD levels. This TCDD uptake was recent and
occurred decades after spraying ended. We hypothesize that a major route
of current and past exposures is from the movement of dioxin from soil into
river sediment, then into fish, and from fish consumption into people.
(Schecter et al. 2001, 435)
“We have a public-health crisis for the people living in Bien Hoa
City,” said Arnold Schecter, a leader in study of dioxin levels in Viet-
nam (“Dioxin Levels” 2001, 4). “We’re seeing increasing dioxin levels
in people now compared to what I was seeing in the 1980s,” Schecter
said. “I would regard this as an emergency” (Verrengia and Tran
2000).
Schecter, who began his Vietnam dioxin studies in 1984, served
in the U.S. Army Medical Corps during the Vietnam War. Schecter
has visited Vietnam sixteen times since then. He believes that the
extensive use of Agent Orange during the war has made Vietnam
today the world’s number-one hot spot for dioxin contamination.
His studies at Bien Hoa are only one example of a plague of dioxin-
induced toxicity that still afflicts many people in Vietnam.
Thanh Xuan, a “peace village” near Hanoi, houses a hundred chil-
dren who are retarded, some with stunted limbs or twisted spines.
Most arrive at the peace village unable to walk, speak, or read.
Across Vietnam, rates of birth defects, miscarriages, and other com-
plications are still uncommonly high almost three decades after
spraying of Agent Orange ended during 1971. Many of the deformed
children in the peace village were born to parents who were sprayed
during the war.
“If I wasn’t here, I don’t know what I would do,” lamented Nguyen
Kim Thoa, fifteen, sitting in her bedroom beneath a Britney Spears
30 The Dirty Dozen
poster. A reporter described Thoa’s delicate features, “wrapped in a

shroud of spongy skin tumors and charcoal splotches sprouting
bristles” (Verrengia and Tran 2000). “I wasn’t able to go to school at
home,” Thoa said. “The children always made fun of me. In their
eyes, I was a freak. Here, I have friends and teachers who love me”
(Verrengia and Tran 2000). Thoa’s father served in the South Viet-
namese Army between 1978 and 1980 along the Cambodian border,
an area that was heavily sprayed during the war.
Hoang Dinh Cau, chairman of a national Vietnamese panel that
investigates the war’s ongoing health consequences, estimates that
about 1 million Vietnamese people are afflicted with dioxin poison-
ing, including 150,000 children. Thirty years after the war some rice
paddies that were abandoned after spraying have not been re-
claimed, as “soaring forests with 1,000 different tree species shriv-
eled, replaced by weedy meadows that livestock won’t graze.
Farmers call the new growth ‘American grass’” (Verrengia and Tran
2000).
In a sparsely decorated bedroom of a two-story concrete building,
Bui Dinh Bi recalls his days with communist forces in Quang Tri,
in what was then called South Vietnam. During the early 1970s,
after he was exposed to Agent Orange, Bui’s skin lesions changed
from mosquito-bite-like bumps to tumors that cover his body thirty
years later. Bui and his wife had eight children. The first was still-
born, and then the next five died in infancy. Their two surviving
children are mentally retarded (O’Neill 2000). Bui lives with twenty-
nine other veterans and seventy children in Friendship Village, near
Hanoi, one of about a dozen similar communities that the Vietnam-
ese government has established for veterans and children afflicted
with dioxin toxicity.
The Washington Post reported in April 2000 that “Canadian re-
searchers have found high levels of dioxins in children that were
born long after the spraying ceased in 1971. The lingering contam-
ination is so severe in some areas that if they were in the United
States, they would be declared Superfund sites, requiring an im-
mediate cleanup effort” (O’Neill 2000).
Malformed children, such as the ones at Friendship Village,
should be very carefully studied before conclusions are drawn link-
ing dioxin to them, Schecter said. To date, the studies performed,
according to Schecter, “have been hypothesis-generating, but not
conclusive” (O’Neill 2000). Crippling birth defects seen across Viet-
nam should not be blamed wholesale on Agent Orange, and may be

due to conditions such as polio, encephalitis, and cerebral palsy,
Schecter said (O’Neill 2000).
Le Cao Dai, who worked with Schecter during his research trips,
has no such reservations. He said that Agent Orange has become
part of the food chain for the people of South Vietnam—affecting
their water and food supply—and remains a problem today. The
directors of Friendship Village say all the veterans were exposed and
all the children’s parents served in South Vietnam during the war
(O’Neill 2000).
DIOXIN SPILL AT SEVESO, ITALY (1976)

On July 10, 1976, a chemical reaction went out of control and
provoked an explosion at the Industrie Chimiche Meda Societa
Arionaria (Icmesa) trichlorophenol manufacturing plant in the
northern Italian town of Seveso, pumping clouds of dioxins from the
subsidiary of the chemical giant Hoffman La Roche.
One source observed that “The local people knew of the explosion
[at Seveso] because of the noise, followed by a reddish-brown cloud
with a nasty smell” (Cook and Kaufman 1982, 10). Other accounts
say the dioxin resembled snow so much that children rushed out of
doors to play in it. Birds at Seveso, according to another eyewitness
account, “literally fell out of the sky and off branches, contorted in
death” (Cook and Kaufman 1982, 11). Domestic cats were found
“swollen and half paralyzed. . . . Dogs vomited green froth and de-
veloped skin eruptions that looked like burns.” The following early
autumn, “two women who had been in the crucial [exposure] Zone
A, nearest to the explosion, gave birth to babies with virtually no
brain tissue.” Both children died (Cook and Kaufman 1982, 11).
The plant’s accidental plume consisted of nearly pure dioxin. Four
days after the dioxin release, flowers and other plants began to
wither and die in Seveso. Birds, fish, and other animals were re-
ported to be dying in abnormally large numbers. Eight days after
the dioxin release, word went out from Seveso seeking medical doc-
tors from all points of the compass as the town’s hospitals over-
flowed with hundreds of ailing people. Their dioxin-dusted homes
had become uninhabitable. Many pregnant women were faced with
having deformed children, or seeking an abortion against the
wishes of the Catholic Church (Hynes 1989, 13).
32 The Dirty Dozen
The 1976 dioxin spill near Seveso, Italy, resulted in the highest
levels of the chemical ever recorded in humans. Its aftermath pro-
duced the first studies to confirm that elevated dioxin levels per-
sisted in people from the exposed areas almost twenty years after
the accident. The same study also found that women experienced
higher dioxin levels than men, portending harm to mothers’ off-
spring.
LOVE CANAL BECOMES A TOXICOLOGICAL

HOUSEHOLD WORD
During the 1940s, Hooker Chemical Corporation used the Love
Canal area (north of Buffalo, New York, along a body of water up-
stream from Niagara Falls) as a dumping ground for a variety of toxic
wastes amounting to 20,000 tons, some of which contained dioxin
contamination. During the early 1950s the contaminated area was
covered with a clay cap that was supposed to seal the contaminants
underground. The land was sold by Hooker Chemical, and, over the
next few years, became the site of several hundred family homes
and a school.
During construction, the clay cap was breached, at the same time
that highway construction disrupted water flow around the site.
Shortly thereafter, several homeowners noted a foul mixture of tox-
ins oozing into their basements. After direct appeals to government
agencies brought little help, the residents of Love Canal organized
public protests that attracted considerable media attention.
In 1978 President Jimmy Carter declared Love Canal a federal
disaster area, the first such declaration for a human-induced en-
vironmental disaster. The government proposed to buy the 200
houses nearest the dump site, but residents were not happy with
the proposed settlement. During 1980, residents took two Environ-
mental Protection Agency officials hostage for several hours. The
number of homes to be purchased was then raised to about 700. In
the meantime, Love Canal became a toxicological household word.
TIMES BEACH, MISSOURI, CEASES TO EXIST

During the late 1960s and early 1970s, waste hauler Russell Bliss
was hired to oil the dusty roads of Times Beach, Missouri, twenty-
five miles southwest of St. Louis, off Interstate 44. Bliss unknow-
ingly mixed dioxin-contaminated waste with the oil that he used for
dust control on several sites, including some of the roads and sta-
bles in Times Beach and twenty-six other eastern Missouri sites
that later were identified as dioxin “hot spots” by the EPA. Bliss used
waste from several companies, including a Verona, Missouri, plant
that had been purchased by Agribusiness Technologies’ parent
company, Syntex Agribusiness. The plant made hexachlorophene,
an antibacterial agent.
During 1982, the EPA took random soil samples at various sites
in Missouri to test for dioxin levels and found, late in the year, what
the agency considered to be dangerous levels of dioxin in the soil at
Times Beach. The 2,240 citizens of Times Beach found themselves
sitting on one of the most toxic patches of earth in the United States.
In February 1983 the EPA announced a buyout of the entire town,
for almost $33 million. The federal government permanently closed
the city after it was discovered that dioxin had contaminated the
town as a by-product of chemical processing and incineration, as
well as Bliss’ spraying. The town was listed as a Superfund site and
demolished in 1992. Cleanup of the site was finished in 1997.
During 1990 the state of Missouri, the EPA, and Agribusiness
Technologies agreed to incinerate dioxin-contaminated material at
Times Beach. The decision called for incineration at Times Beach
of dioxin-contaminated soils from several sites. Times Beach had
been a ghost town since 1983, when it was purchased using Su-
perfund monies. Syntex was held responsible and estimated the
work would take five to seven years. Syntex also agreed to pay the
government $10 million to reimburse some of the government’s
costs in the case.
The decision to incinerate Times Beach’s dioxin-laced soil
sparked opposition, and six years of delays, from some environ-
mental groups. On March 17, 1996, the incinerator began opera-
tion; by mid-June 1997, 265,354 tons of soil and other
dioxin-contaminated material from Times Beach and twenty-six
other sites in eastern Missouri had been incinerated. David Shorr,
director of the Missouri Department of Natural Resources, said that
the cost of the Times Beach cleanup was about $200 million (Man-
sur 1997).
The incineration may have removed dioxin from the soil of what
used to be Times Beach. Taking a planetwide inventory, however,
the dioxin was merely displaced, given up to the winds and waters,
34 The Dirty Dozen
and lodging, perhaps, eventually in the milk of an Inuit mother, or

that of a polar bear. Pat Costner, a Greenpeace scientist, said that
neither the EPA nor its state counterparts denied that some un-
known quantity of dioxin was dispersed by the incinerator into the
environment.
“That’s contrary to protecting the public’s health or the environ-
ment,” Costner said. “Now we’ll just have to watch and wonder for
decades” about the effect of the dioxin dispersal, Costner said.
“That’s what is left now” (Mansur 1997).
Within two months after Times Beach shut down its incinerator,
dioxin was discovered in the soil in west St. Louis County—this time
in the suburb of Ellisville. Officials with the EPA said that a private
driveway in Ellisville had been found to have dioxin levels as high
as 195 parts per billion. In a statement, the agency said dioxin levels
more than 1 part per billion are “of concern” (Allen 1997b).
A SUPERFUND SITE ON THE HUDSON

In 1983, the same year that Times Beach became uninhabitable,
two hundred miles of the Hudson River were declared a Superfund
hazardous-waste site. The EPA ordered GE to dredge thirty years’
worth of PCBs from a thirty-five-mile stretch of the river. The com-
pany had discharged PCBs into the Hudson from manufacturing
plants in Fort Edward and Hudson Falls between 1947 and 1977.
Between Albany and Fort Edward, two GE capacitor plants dumped
more than 1 million pounds of PCBs into the Hudson River before
PCBs were outlawed in 1977.
The EPA in early August 2001 ordered GE to pay $480 million to
dredge toxic chemicals, mainly PCBs, off the floor of the upper Hud-
son River. This was the costliest environmental cleanup in the
United States to that time.
The anticipated cleanup will last more than five years and involve
“dredging 2.65 million cubic yards of contaminated sediment along
a picturesque 37-mile run of the Hudson River” (Powell 2001, A-5).
Dredging of the Hudson was being planned with machinery that
sucks up contaminated sludge and water. One account described
the scope of the project:
The dredging, slated to start in 2003, will be epic in sweep. Dredgers will
ply the river’s waters, at least two processing plants will be built on the river
or its banks to separate the PCBs, and a stream of trains and trucks will
haul thousands of pounds of the foul-smelling stuff to presumably distant

landfills. Once that is completed, the dredgers will lay down thousands
more tons of clean sediment on the riverbed to cover remaining PCBs and
begin restoration of the natural habitat. (Powell 2001, A-5)
Before the EPA order, GE officials spent at least $15 million on an

advertising and lobbying campaign against dredging. GE officials
asserted that the safer course, not to mention the less expensive
one, would be to let natural sediments inexorably entomb the PCBs
on the riverbed. The river is vastly cleaner than it was three decades
ago, and GE officials note that thousands now swim in the river and
at least one town in the affected region—Waterford, New York—taps
the river for drinking water (Powell 2001, A-5).
The company spent millions of dollars on lobbying and advertis-
ing, in an abortive attempt to persuade state and federal officials
that the dredging project, which will remove roughly 150,000
pounds of PCB-laced sediments from the river’s bed, is unnecessary
and environmentally risky (Lazaroff 2001).
During August 2001, GE said that massive dredging would “cause
more harm than good” (Lazaroff 2001). “This is a loss for the people
of the area who overwhelmingly oppose this project and the decades
of disruption it will bring to their communities,” GE said in August.
“It appears that neither sound science nor the voices of these resi-
dents played a part in the EPA’s decision” (Lazaroff 2001). GE has
argued that the EPA’s cleanup plan would “resuspend” PCBs now
buried in river sediments, thereby releasing additional toxins into
the environment. In sticking by its original plan, the EPA has re-
jected that argument (Lazaroff 2001).
According to plans presented during December 2001, the design
phase of the dredging project is expected to take about thirty-six
months, and the EPA may adjust the plan after reviewing data col-
lected during this phase. As part of the process, the EPA will solicit
public input on issues including the location for the initial dredging
and the type of equipment to be used. The dredging itself could take
at least five years (Lazaroff 2001). During April 2002 GE said it
would comply with the EPA order.
OPPOSITION TO POPS GALVANIZES

Even before an explosion of DDT use in the late 1940s, scientists
at the U.S. Fish and Wildlife Research Center in Laurel, Maryland,
36 The Dirty Dozen
published papers establishing its toxicity to wildlife from sprays at

high rates of application (5 pounds per acre) (Marco, Hollingsworth,
and Durham 1987, 85–87). The nature of this toxicity remained un-
known to the general public until publication of Rachel Carson’s
Silent Spring in 1962. Pest resistance to DDT also became public
knowledge with the publication of Silent Spring, but knowledge
of resistance in Italian houseflies was noted in small-circulation
scientific journals as early as 1948 (Marco, Hollingsworth, and
Durham 1987, 120). Similarly, the persistent nature of certain
synthetics (notably DDT and PCBs) was known to science by the
middle 1960s, long before public knowledge forced their restriction,
regulation, and eventual elimination.
During 1987, the Conservation Foundation (Washington, D.C.)
and the Institute for Research on Public Policy (Ottawa, Ontario)
convened a team of scientists to study the ecological condition of
the Great Lakes and their watersheds. This study included effects
of synthetic chemicals on wildlife. A book, Great Lakes/Great Leg-
acy? (1990) was based on the proceedings of this conference; it
asserted that “chemical contamination was associated with the
widespread reproductive failure of wildlife within the watershed,
particularly that of fish and fish-eating birds and mammals” (Krim-
sky 1999, 16).
At about the same time, Theo Colborn, who had compiled a lit-
erature search for the Great Lakes/Great Legacy project, was begin-
ning to draw together the scientific threads that would establish the
study of synthetic toxins’ endocrinal effects. Colborn convened sev-
eral conferences that brought together experts in biology, biochem-
istry, toxicology, and zoology, as she began to weave information
from diverse sources into a pattern that linked incomplete sexual
development of fish in the Great Lakes with increasing wildlife ste-
rility, thyroid abnormalities, and declining rates of survival in sev-
eral bird species in the same watershed. “From these observations,”
wrote Sheldon Krimsky, “she advanced a generalized causal hy-
pothesis, suggesting that the pervasive presence of chemical endo-
crine disruptors introduced into the environment was responsible
for the reproductive abnormalities found in wildlife populations”
(Krimsky 1999, 20).
The first of a series of meetings convened by Colborn during July
1991, with financial assistance from the W. Alton Jones Founda-
tion, was titled “Chemically Induced Alterations in Sexual and
Functional Development: The Wildlife/Human Connection.” Known

to its participants as “Wingspread I” the conference ended with a
consensus statement signed by twenty-one participants that as-
serted that a large number of human-manufactured chemicals had
been injected into the environment, that these chemicals are bioac-
cumulative across generations and along food chains, and that
these chemicals, by mimicking estrogen, were interfering with the
functioning of many species’ endocrine systems.
Colborn recalls being surprised at what seemed, at the time, the
consummate implausibility of the connections she and the others
were uncovering, wondering whether many people would believe
what seemed like the plot of a science-fiction novel. The Wingspread
I consensus statement went on to list several specific ways in which
endocrine-disrupting chemicals have been shown to disrupt repro-
duction in several species of animals.
THE CHLORINE CHEMISTRY COUNCIL IS

CREATED
The Chlorine Chemistry Council, created in 1993 by the Chemical
Manufacturers Association, advocates use of chlorine compounds
in industry and agriculture. It maintains that dietary elements
(dairy products and soya) are causing increasing estrogen loads in
people’s bodies more than synthetic industrial chemicals. Accord-
ing to the CCC (known colloquially as “c-cubed”) human intake of
natural estrogens is “several orders of magnitude” above the con-
tribution of synthetic toxins (Krimsky 1999, 101).
Started during the mid-1990s, the Chemical Industry Institute of
Technology, “a respected research institute that is heavily sup-
ported by major chemical companies,” (Krimsky 1999, 164) was
spending about $1.5 million annually investigating the environ-
mental endocrine hypothesis.
HOW TO POISON A NATION’S FOOD WEB: THE

CASE OF BELGIUM, 1999
An example of how easily one accident can imperil the food web
of an entire nation was provided by Belgium during 1999 as animal
feeds become contaminated with PCB-laced oils. As a result of this
contamination, chickens were contaminated at levels up to 5,000
38 The Dirty Dozen
times safety levels. Not all the chickens were for human consump-
tion; some were used for breeding chicks, contaminating egg sup-
plies as well.
Belgium quarantined about a thousand poultry and pig farms
during the summer of 1999, following detection of dioxin contami-
nation, after tests revealed PCBs, which can indicate the presence
of dioxins in animal feed. Dioxin was introduced into the Belgian
food supply through contaminated animal fat used in animal feeds
supplied to Belgian, French, and Dutch farms. Hens, pigs, and cat-
tle ate the contaminated feed.
The feed was supplied by the Versele company, which used animal
fat from Verkest, one of two fat processors identified as the source
of a dioxin contamination episode in Belgium the previous May. Fat
processor Fogra also was implicated in the original contamination.
Dioxin contamination prompted bans on sales of Belgian meat,
chicken, eggs, dairy products, and processed foods in several other
countries.
The Belgian government’s initial reluctance to reveal the severity
of the contamination caused political upheaval that led voters to
defeat the incumbent coalition government in elections held during
June 1999. The crisis reportedly cost the Belgian economy more
than $1.5 billion in lost revenue (Handyside 1999). The government
of Belgium was forced to repurchase and destroy pork and pro-
cessed pork foods with a fat content of more than 20 percent that
may have been contaminated.
Investigations later revealed that Belgian authorities had known
of the contamination since mid-March; the high dioxin levels had
been confirmed on April 26, a month before the government made
the information public. Only on May 28, 1999, did the Belgian pub-
lic health minister announce a ban on the sale of dioxin-laced chick-
ens and eggs.
Contaminated fat had been used to manufacture animal feed by
Verkest as early as late January 1999. The contaminated feed was
supplied to eight other Belgian animal-feed manufacturers, as well
as one each in France and the Netherlands. The same feed was then
sold to egg, broiler chicken, pork, and beef producers.
On May 26, test results revealed high levels of dioxins in laying
hens at farms receiving feed from the implicated animal-feed pro-
ducers, indicating that chickens and eggs sold during April had con-
tained high levels of dioxins. Beginning on May 27, the 417 poultry
farms that had bought feed from these nine suppliers were placed
under surveillance. Their products were traced. On May 28 the Bel-
gian public health minister ordered removal of all chicken and eggs
from store shelves and cautioned the public against eating Belgian
poultry and eggs (Lok and Powell 2000).
The initial ban was extended by the government on June 1 to
include a ban on sale of all products containing chicken or eggs until
they were inspected. Slaughter and transport of cattle, pigs, and
poultry were prohibited. A preliminary list of all poultry and later
pork and beef farms using feed originating directly or indirectly from
Verkest was assembled and updated on a regular schedule. As the
number of banned foods grew, the agriculture and public health
ministers of the Belgian government resigned on June 1 (Lok and
Powell 2000). At least thirty countries (including Canada, Australia,
Hong Kong, Taiwan, Russia, Egypt, Algeria, South Africa, Poland,
Switzerland, most European Union countries, and several other
non–European Union countries) temporarily banned imports of Bel-
gian agricultural products (Lok and Powell 2000).
On June 2, the European Union directed member nations to re-
move and destroy all animal feed, poultry, and egg products that
might contain dioxins, as well as “other products containing more
than 2 percent egg product produced by the suspect farms between
January 15 and June 1” (Lok and Powell 2000). Throughout June,
countries across Europe quit selling all Belgian egg and poultry
products. The same day, two Verkest executives, father and son,
were arrested and charged with fraud and falsification of documents
that prosecutors said “misled customers [into] thinking they were
buying 100 percent animal fat” (Lok and Powell 2000). The accused
denied that they had deliberately contaminated the suspect animal
feed.
The European Community on June 4 extended its restrictions to
include products derived from livestock other than poultry (includ-
ing milk and dairy products) from suspect farms. On June 10, angry
Belgian farmers blockaded roads at the Dutch and French borders
in protest against the export bans.
Belgian officials arrested two executives from Fogra on June 23.
A public prosecutor said Fogra was the initial source of contami-
nation, having dioxins and PCBs in its products and suggested that
motor oil there had been mixed with frying fat. On July 14, inves-
tigators said they were almost sure that oil from an electrical trans-
40 The Dirty Dozen
former somehow had found its way into old cooking oil that was
recycled into fat for animal feed (Lok and Powell 2000).
As problems related to tainted animal feed spread across Europe,
media reports provided Belgians with discomforting detailed reports
describing in graphic detail the process by which animal fat is pro-
cured for feed. Reporters found that fat-processing plants routinely
collected used fat from municipal recycling facilities where consum-
ers disposed of used motor oils along with other household wastes.
The plants also accept used fat and oil from restaurants and indus-
trial food plants, which filter, cook, and sterilize it. The recycled fat
was then shaped into blocks and sold to animal-feed manufactur-
ers. Some reports speculated that dioxin-tainted transformer oil
was illegally dumped into cooking oil somewhere in this process.
On June 30, the Belgian government said that such problems had
cost the nation’s economy US$1.54 billion, half from the agricul-
tural sector and the other half from other food industry (“Belgium
Sees” 1999). On July 23, 233 more pig farms were quarantined after
two of them reported PCB levels up to fifty times allowable limits.
Several Belgian scientists wrote an article in the scientific journal
Nature contending that, given usual consumption patterns, most
people who ate food produced in Belgium would not suffer PCB-
related harm (Bernard et al. 1999, 231).
Dioxin contamination during these years was not limited to
Belgium. Contaminated citrus pulp pellets from Brazil in animal
feed caused dioxin contamination of milk in Germany during late
1997 and early 1998. Some milk had levels greater than national
safety limits. The citrus pulp also was used as animal feed in eleven
other European countries. About 92,000 tons of citrus pulp pellets
had to be thrown away. The contamination arose from dioxin-
contaminated waste lime produced as a by-product by the Solvay
company in Brazil. The waste lime is converted into a form that is
then added to citrus pulp for animal feed.
LOCAL PROTESTS RISE

Protests of POPs’ toll may erupt anyplace with a significant point-
source of the chemicals, usually from a factory’s smokestacks or
waterborne wastes. Incinerators are favorite targets. For example,
during the summer of 2001 activists stepped up their protests at an
East Oakland, California, medical waste incinerator, blocking its
access roads until they were arrested and carried away by police.
Local environmentalists and community activists have been pro-
testing at Integrated Environmental Systems, the state’s only com-
mercial medical-waste incinerator, claiming it emits cancer-causing
dioxin and other hazardous chemicals into the air. Incinerator of-
ficials deny their operations pose a health risk to the community,
contending that their emissions are well below state and federal
standards.
“Yesterday,” wrote a reporter for the San Francisco Chronicle on
August 7, 2001, “was the first time protesters attempted to disrupt
incinerator operations by keeping trucks carrying waste from en-
tering or leaving the facility, just off Interstate 880 on High Street.
The group, which numbered about 70 people before dwindling to
fewer than 40, did allow a few trucks to pass through, but said there
were far fewer than normal” (DeFao 2001, A-16). Several protesters
said they live within a mile of the plant and fear for their health.
“Today is the beginning of the end of incineration,” said Bradley
Angel of Greenaction in San Francisco, one of the protest leaders.
“If the government won’t do it, the people will” (DeFao 2001, A-16).
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2
“We Feel like an Endangered Species”:
Toxics in the Arctic
“As we put our babies to our breasts we are feeding them a noxious,
toxic cocktail,” said Sheila Watt-Cloutier, a grandmother who also
is Canadian president of the Inuit Circumpolar Conference (ICC).
“When women have to think twice about breast-feeding their babies,
surely that must be a wake-up call to the world” (Johansen 2000,
27). Watt-Cloutier was raised in an Inuit community in remote
northern Quebec. She didn’t know it at the time, but toxic chemicals
were being absorbed by her body and by those of other Inuit in the
Arctic.
Watt-Cloutier now ranges between her home in Iqaluit (pro-
nounced “ee-ha-loo-eet,” capital of the new semisovereign Nunavut
Territory) to and from Ottawa, Montreal, New York City, and other
points south, doing her best to alert the world to toxic poisoning and
other perils faced by her people. The ICC represents the interests of
roughly 140,000 Inuit spread around the North Pole from Nunavut
(which means “our home” in the Inuktitut language) to Alaska and
Russia. Nunavut itself, a territory four times the size of France, has
a population of roughly 27,000, 85 percent of whom are Inuit.
Many residents of the temperate zones hold fond stereotypes of a
pristine Arctic largely devoid of the human pollution that is so ubiq-
uitous in their lives. To a tourist with no interest in environmental
toxicology, the Inuit Arctic homeland may seem as pristine as ever
during its long, snow-swept winters. Many Inuit still guide dogsleds
onto the pack ice surrounding their Arctic-island homelands to
hunt polar bears and seals. Such a scene may seem pristine, until
one realizes that the polar bears’ and seals’ body fats are laced with
dioxins and PCBs.
48 The Dirty Dozen
The toxicological due bills for modern industry at the lower lati-
tudes are being left on the Inuit table in Nunavut, in the Canadian
Arctic. Native people whose diets consist largely of sea animals
(whales, polar bears, fish, and seals) have been consuming concen-
trated toxic chemicals. Abnormally high levels of dioxins and other
industrial chemicals are being detected in Inuit mothers’ breast
milk.
To the naked eye, the Arctic still looks pristine. In Inuit country
these days, however, it’s what you can’t see that may kill you:
• Persistent organic pollutants (“POPs” to environmental toxicologists),
such as DDT, dioxins, and PCBs, are multiplying up the food chain of the
Inuit as air and ocean currents transport the effluvia of southern industry
into polar regions. Geographically, the Arctic could not be in a worse posi-
tion for toxic pollution, as a ring of industry in Russia, Europe, and North
America pours pollutants northward. POPs have been linked to cancer,
birth defects, and other neurological, reproductive, and immune-system
damage in people and animals. At high concentrations, these chemicals also
damage the central nervous system. Many of them also act as endocrine
disrupters, causing deformities in sex organs as well as long-term dysfunc-
tion of reproductive systems. POPs also can interfere with the function of
the brain and endocrine system by penetrating the placental barrier and
scrambling the instructions of the naturally produced chemical messen-
gers. The latter tell a fetus how to develop in the womb and postnatally
through puberty; should interference occur, immune, nervous, and repro-
ductive systems may not develop as programmed by the genes inherited by
the embryo.
• Global warming is accelerating more quickly in the Arctic than any-
where else on Earth; some Inuit villages are being washed into the sea or
slowly swallowed by melting permafrost as shrinking sea ice imperils the
survival of some species. Sand flies have been seen on Banks Island in the
high Arctic. Several Inuit have fallen through thin ice, usually on snow-
mobiles, and died. Residents of Banks Island, above the Arctic Circle, tell
of experiencing thunder, lightning, and hail for the first time in anyone’s
memory.
• Atmospheric chemistry in the stratosphere is accelerating ozone deple-
tion over the Arctic (see also chapter 3), threatening the Inuit and animals
with cancer from ultraviolet radiation. Some elders and hunters in Iqaluit
have reported physical abnormalities afflicting the seals they catch, includ-
ing some seals without hair, “and seals and walruses with burn-like holes
in their skin” (Lamb n.d.).
Welcome to ground zero on the road to environmental apocalypse:

a place, and a people, who never asked for any of the curses that
‘‘We Feel like an Endangered Species’’ 49
industrial societies to the south have brought to them. The bevy of

environmental threats facing the Inuit are entirely outside their his-
torical experience.
“We are the miner’s canary,” says Watt-Cloutier. “It is only a mat-
ter of time until everybody will be poisoned by the pollutants that
we are creating in this world” (Lamb n.d.). “At times,” said Watt-
Cloutier, “We feel like an endangered species. Our resilience and
Inuit spirit and of course the wisdom of this great land that we work
so hard to protect gives us back the energy to keep going” (Sheila
Watt-Cloutier, personal communication, March 28, 2001).
Most the chemicals that now afflict the Inuit are synthetic com-
pounds of chlorine; some of them are incredibly toxic. For example,
one-millionth of a gram of dioxin will kill a guinea pig (Cadbury
1997, 184). Scan the list of scientific research funding around the
world and add up what ails the Arctic. In addition to a plethora of
studies documenting the spread of persistent organic pollutants
through the flora and fauna of the Arctic, many studies aim to doc-
ument the saturation of the same area by levels of mercury, lead,
and nuclear radiation in fish and game (PD 2000 Projects 2001).
Following is a sampling of titles for research projects directed at
documenting the ongoing eco-tastrophe in the Arctic. The destruc-
tion of Arctic’s ecosystem is certainly being well documented. The
studies have been generated by scientists in the United States, Can-
ada, Sweden, Norway, and Russia (PD 2000 Projects 2001).
“New Persistent Chemicals in the Arctic Environment”

“Retrospective Survey of Organochlorines and Mercury in Arctic Seabird
Eggs”
“Effects of Prenatal Exposure to Organochlorines and Mercury in the Im-
mune System of Inuit Infants”
“Estimation of Site Specific Dietary Exposure to Contaminants in Two Inuit
Communities”
“Follow-up of Pre-school-aged Children Exposed to PCBs and Mercury
through Fish and Marine Mammal Consumption”
“Temporal Trends of Persistent Organic Pollutants and Metals in Ringed
Seals of the Canadian Arctic”
“Assessment of Organochlorines and Metal Levels in Canadian Arctic Fox”
“Effects and Trends of POPs on Polar Bears”
“Contaminants in Greenland Human Diet”
50 The Dirty Dozen
“Lead Contamination of Greenland Birds”

“UV-Radiation and Its Impact on Genetic Diversity, Population Structure,
and Foodwebs of Arctic Freshwater”
“Effects of Metals and POPs on Marine Fish Species”
“Heavy Metals in Grouse Species”
“Endocrine Disruption in Arctic Marine Mammals”
“Persistent Toxic Substances, Food Security, and Indigenous Peoples of the
Russian North”
“Metals in Reindeer”
“Concentrations and Patterns of Persistent Organochlorine Contaminants
in Beluga Whale Blubber”
“Ultraviolet (UV) Monitoring in the Alaskan Arctic”
The bodies of some Inuit, thousands of miles from the sources of

the pollution, have the highest levels of PCBs ever detected, except
in victims of industrial accidents. Some native people in Greenland
have more than seventy times as much of the pesticide hexacloro-
benzene (HCB) in their bodies as temperate-zone Canadians (Jo-
hansen 2000, 27).
Pesticide residues in the Arctic today may include some used de-
cades ago in the southern United States. The Arctic’s cold climate
also slows decomposition of these toxins, and so they persist in the
Arctic environment longer than at lower latitudes. The Arctic acts
as a cold trap, collecting and maintaining a wide range of industrial
pollutants, from PCBs to toxaphene, chlordane to mercury, accord-
ing to the Canadian Polar Commission (PCB Working Group, n.d.).
As a result, “Many Inuit have levels of PCBs, DDTs and other per-
sistent organic pollutants in their blood and fatty tissues that are
five to ten times greater than the national average in Canada or the
United States” (PCB Working Group, n.d.).
Generation of POPs has become an issue in Watt-Cloutier’s home,
Iqaluit, on Baffin Island, where the town dump burns wastes that
emit dioxins and furans. The dump’s plume provides only a small
fraction of Iqaluit residents’ POP exposure, but it has become
enough of an issue to figure in a three-month shutdown of the dump
that caused garbage to pile up in the town. The dump was reopened
after local public-health authorities warned that the backlogged
garbage could spread disease and that “the hazard posed by the
rotting piles of garbage outweighed the risks of burning it” (Hill
2001, 5). In 2001 Iqaluit’s government was asking residents to sepa-

rate plastics and metals from garbage that can be burned without
adding POPs to the atmosphere.
Dioxin, PCPs, and other toxins accumulate with each succeeding
generation in breast-feeding mammals, including the Inuit and
many of their food sources. The reproductive cycle of humans and
other mammals compounds the toxic effects of these chemicals. Air-
borne toxic substances are absorbed by plankton and small fish,
which are then eaten by dolphins, whales, and other large animals.
The mammals’ thick subcutaneous fat stores the hazardous sub-
stances, which are transmitted to offspring through breast-feeding.
Sea mammals are more vulnerable to this kind of toxicity than land
animals, and so the levels of chemicals in their bodies can reach
exceptionally high levels. The level of these toxins increases with
each breast-fed generation.
INUIT INFANTS “A LIVING TEST TUBE FOR

IMMUNOLOGISTS”
Inuit infants have provided “a living test tube for immunologists”
(Cone 1996, A1). Due to their diet of contaminated sea animals and
fish, Inuit women’s breast milk contains six to seven times the PCB
level of women in urban Quebec, according to Quebec government
statistics. Their babies have experienced strikingly high rates of
meningitis, bronchitis, pneumonia, and other infections compared
with other Canadians. One Inuit child out of every four has chronic
hearing loss due to infections.
“In our studies, there was a marked increase in the incidence of
infectious disease among breast-fed babies exposed to a high con-
centration of contaminants,” said Eric Dewailly, a Quebec Public
Health Center researcher and Laval University scientist who was
among the first scientists to detect high levels of POPs in the bodies
of Inuit mothers and their breast milk (Cone 1996, A1). Born with
depleted white blood cells, Inuit children suffer excessive bouts of
diseases, including a twentyfold increase in life-threatening men-
ingitis compared to other Canadian children. These children’s im-
mune systems sometimes fail to produce enough antibodies to
resist even the usual childhood diseases. A study published Sep-
tember 12, 1996, in the New England Journal of Medicine (Jacobson
and Jacobson 1996, 783–89) confirmed that children exposed to
52 The Dirty Dozen
low levels of PCBs in the womb grow up with low IQs, poor reading
comprehension, difficulty paying attention, and memory problems.
According to the Quebec Health Center, a concentration of 1,052
parts per billion (ppb) of PCBs has been found in Arctic women’s
milk fat. This compares to a reading of 7,002 ppb in polar bear fat,
1,002 ppb in whale blubber, 527 ppb in seal blubber, and 152 ppb
in fish. The U.S. Environmental Protection Agency safety standard
for edible poultry, by contrast, is 3 ppb and in fish, 2 ppb. At 50
ppb, soil is often considered to be hazardous waste.
Research by the Canadian federal department of Indian and
Northern Affairs indicates that Inuit women throughout Nunavut
have DDT levels nine times that of averages in Canadian urban ar-
eas. Milk of Inuit women of the Eastern Arctic has been measured
to contain as much as 1,210 ppb of DDT and its derivative, DDE,
while milk from women living in southern Canada contains about
170 ppb (Suzuki 2000).
Although the United States is thousands of kilometers from its
borders, Nunavut receives up to 82 percent of its dioxins from in-
dustries there (Suzuki 2000). Some of the pollution in the Canadian
Arctic arrives from as far away as Western Europe and Japan. Con-
taminants can reach the Canadian Arctic from Europe in two weeks.
Dewailly accidentally discovered that Inuit infants were being
heavily contaminated by PCBs. During the middle 1980s, Dewailly
first visited the Inuit seeking a pristine group to use as a baseline
with which to compare women in southern Quebec who had PCBs
in their breast milk. Instead, Dewailly found that Inuit mothers’
PCB levels were several times as high as the levels of the Quebec
mothers in his study group.
Dewailly and colleagues (Dewailly, Ayotte, et al. 2000; Dewailly,
Bruneau, et al. 1993; Dewailly, Dodin, et al. 1993; Dewailly, Ryan,
et al. 1994) then investigated whether organochlorine exposure is
associated with the incidence of infectious diseases in Inuit infants
from Nunavut. Dewailly and colleagues (Dewailly, Bruneau, et al.
1993, 403–6) reported that serious ear infections were twice as com-
mon among Inuit babies whose mothers had higher than usual con-
centrations of toxic chemicals in their breast milk. More than 80
percent of the 118 babies studied in various Nunavut communities
had at least one serious ear infection in the first year of life (Calamai
2000).
The most common contaminants that researchers found in Inuit
mothers’ breast milk were three pesticides (dieldrin, mirex, and
DDE, a derivative of DDT) and two industrial chemicals—PCBs and

hexachlorobenzene. The researchers could not pinpoint which spe-
cific chemicals were responsible for making the Inuit babies more
vulnerable because chemicals’ effects may intensify in combination.
The Arctic Monitoring and Assessment Program, a joint activity
of Arctic nations and organizations of indigenous Arctic peoples,
said that “PCB blood levels, while highest in Greenland and the
eastern Canadian Arctic, were high enough (over 4 micrograms of
PCBs per liter of blood) that a proportion of the population would
be in a risk range for fetal and childhood development problems”
(PCB Working Group n.d.).
Because they are not easily broken down or excreted, these com-
pounds remain in the body for months or years. In ecosystems, they
tend to concentrate or bioaccumulate in the bodies of animals at
the top of their respective food chains: large meat eaters such as
marine mammals, polar bears, raptors, and human beings. Dol-
phins, seals, and whales in the northern seas are being contami-
nated. Large land animals, such as caribou, also are affected.
“The last thing we need at this time is worry about the very coun-
try food that nourishes us, spiritually and emotionally, poisoning
us,” Watt-Cloutier said. “This is not just about contaminants on our
plate. This is a whole way of being, a whole cultural heritage that is
at stake here for us” (Mofina 2000, A12). “The process of hunting
and fishing, followed by the sharing of food—the communal partak-
ing of animals—is a time-honored ritual that binds us together and
links us with our ancestors,” said Watt-Cloutier (PCB Working
Group, n.d.).
In many cases, the Inuit have no practical alternative to “country
food.” Although grocery stores do business in Canadian Inuit ham-
lets today, all the food is flown in. No roads or natural land bridges
lead south from the villages. The cost of air freight, compounded by
distance, raises the cost of a quart of milk in the high Arctic to $4,
and that of a battered head of lettuce to $3. A tiny frozen turkey the
size of a stewing hen may cost $40 in the Arctic.
TOXIC POLLUTION VIA THE DEW LINE

At the same time that Inuit are being poisoned by imported toxins,
they also have discovered that parts of their homelands are laced
with toxic “hot spots” left behind by abandoned military installa-
54 The Dirty Dozen
tions and mines, all also imports from the industrial south. Several
of these hot spots are located at or near the 63 military sites in
Canada, Greenland, and Alaska that make up the Distant Early
Warning (DEW) system of radar sites. At these sites, according to
the Arctic Monitoring and Assessment Program, an estimated thirty
tons of PCBs were used, and “an unknown amount has ended up
in their landfills” (PCB Working group, n.d.).
Under an agreement reached in 1998, Canadian taxpayers, not
the U.S. government, are paying most of the $720 million cleanup
bill for fifty-one decommissioned U.S. military sites across Canada.
Cleanup of cancer-causing PCBs, mercury, lead, radioactive ma-
terials, and various petroleum by-products is expected to take
nearly thirty years. Under the arrangement, the United States was
absolved of legal responsibility for environmental damage in Can-
ada in exchange for $150 million in U.S. weapons and other military
equipment.
The cleanup of all fifty-one American military sites has revealed
pollution that newspaper reports in Canada characterized as “stag-
gering” (Pugliese 2001, B1). For example, at Argentia, Newfound-
land, seventy miles southwest of St. John’s, a large U.S. Navy base,
which opened in 1941 and closed in 1994, left behind PCBs, heavy
metals, and asbestos as well as landfills full of other hazardous
wastes. Waste fuels also have contaminated the water table in the
area.
Abandoned DEW sites in the Arctic were contaminated with dis-
carded batteries, antifreeze agents, solvents, paint thinners, PCBs,
and lead. According to news accounts, “[Canadian] Defence De-
partment scientists have established that PCBs have leaked from
the DEW line sites into surrounding areas as far away as 20 kilo-
meters and, in some cases, the chemicals have been absorbed by
plant and animal life” (Pugliese 2001, B1). Many of the DEW line
locations were established in areas where native people hunt and
fish.
Alaska Community Action on Toxics works with indigenous com-
munities who face toxic contamination from Cold War sites, includ-
ing the Yup’ik community on Saint Lawrence Island. Alaska
Community Action on Toxics also has provided the first compre-
hensive map of more than 2,000 hazardous waste sites in Alaska.
The Inuit also endure pollution from the European and Asian side
of the Arctic Ocean. Pesticide residues and other pollutants spill
into the Arctic Ocean from north-flowing Russian and Siberian

rivers. Decaying Russian nuclear submarine installations on the
White Sea have polluted the ocean with nuclear waste, including
entire reactor cores from scrapped ships.
While many of the former Soviet Union’s worst polluters have gone
out of business, some prosper despite the fact that their effluent is
adding to the Canadian Arctic’s toxic overload. The worst offender
is the Norilsk nickel smelter, in northern Siberia. Traces of heavy
metals from Norilsk’s industries have been detected in the breast
milk of Inuit mothers.
Geoffrey York, a reporter for the Toronto Globe and Mail, described
the industrial city of Norilsk, population 230,000, as “the world’s
most polluted Arctic metropolis” (York 2001, A1).
Looming at the end of the road is a horizon of massive smokestacks, leaking

pipes, rusting metal, gigantic slag heaps, drifting smog, and thousands of
denuded trees as lifeless as blackened matchsticks. Inside malodorous
smelters, Russian workers wear respirators as they trudge through the hot
suffocating air, heavy with clouds of dust and gases. . . . Soviet[era] research
in 1988 found that Norilsk Nickel had created a 200-kilometer corridor of
dead forests to the southeast of the city. (York 2001, A11)
“We, the Inuit, who for a millennia have lived in harmony with,
and with great respect for our land and wildlife, are now most im-
pacted by outside forces such as POPs and climate change,” said
Watt-Cloutier. “With so much already on our plate in terms of at-
tempting to reclaim and restructure our lives to gain back some
control over our lives, be it personal, family, institutions, gover-
nance systems, etc., it can at times be overwhelming” (personal
communication, Mar. 28, 2001).
SOCIOECONOMIC CHANGES IN NUNAVUT

Nunavut could be characterized as the largest “Indian reserva-
tion” in the world. The per capita annual income in Nunavut is about
U.S. $7,000, which doesn’t go far in a place where two liters of milk
costs $7 and a loaf of Wonder bread retails for $3. While most of
Nunavut has few roads and no railroads (communities are con-
nected by regular airline service), all villages now have television
and radio, and most have telephone and the Internet, and so images
imported from the outside world are never far away.
56 The Dirty Dozen
Widespread poverty, unemployment, crime, substance abuse,

and a high suicide rate continue to beset Nunavut, which also faces
22 percent unemployment. Iqaluit (Inuktitut for “fishing place”), the
capital of Nunavut (situated on southeastern Baffin Island about
sixteen hundred miles north of New York City) contains about sixty-
five hundred people, many of whom share big-city problems im-
ported from the outside, including alcoholism, drug abuse, and
AIDS.
The Royal Canadian Mounted Police detachment at Iqaluit has
complained that its members spend so much time rounding up
drunks that “it’s getting in the way of fighting crime” (Iqaluit Drunks
2001).Three thousand incarcerations in the local drunk tank have
been clocked in a year.
The traditional (usually nomadic) Inuit hunting economy endured
largely intact until the 1950s and 1960s, when Canadian authori-
ties forced many people to settle in permanent communities. Many
Inuit children were pressured to attend church-run boarding
schools away from their families. The schools were designed to as-
similate Inuit children into the culture of the qablunaaq, the white
man.
The near-collapse of the hunting economy has coincided with a
sharp rise in suicides. Less than fifty years ago, suicide was virtually
unknown among the Inuit of Canada’s Arctic. Suicide now has be-
come one of the leading causes of death in Iqaluit. Among young
people, suicide has become by far the leading cause of death. Geela
Patterson, adviser to the new territorial government on women’s is-
sues, and herself a suicide-prevention counselor, took her own life
during June 1999. Even in a town with one of the highest suicide
rates in Canada (seven times the Canadian average), where few fam-
ilies have been untouched, Patterson’s death sent shock waves
through the community.
Most of Nunavut’s suicides in recent years have been healthy
young men, aged fifteen to twenty-nine. After the destruction of fur
markets from antifur campaigns in Europe and the United States,
unemployment rates in northern villages have risen more than 50
percent. “When you reduce the usefulness of men in society, it is
bound to have psychological effects,” said Simona Arnatsiaq, leader
of a Baffin Island women’s organization (Brooke 2000).
Susan Aglukark, an Inuit singer who has gained pop-star status
in southern Canada, “sings of the pain caused by suicide in ballads
in English and in her Native Inuktitut” (Brooke 2000). “We are in-
vesting more money for suicide prevention,” said Paul Okalik, whose
brother committed suicide (Brooke 2000). “I myself, when younger
and miserable, have heard the siren call of suicide as a release from
suffering, as has my husband, and others that I know and love,”
Rachel Attituq Qitsualik, wrote in the Nunatsiaq News, a weekly
newspaper serving the eastern Arctic. “My brother gave in to it”
(Brooke 2000).
GLOBAL WARMING: THE ARCTIC WORLD

TURNED UPSIDE DOWN
Global warming is no theory in the Arctic, no subject of debate in
search of (in U.S. President George W. Bush’s words) “sound sci-
ence.” In many areas of the Arctic, unusual warmth in a land that
lives and dies by snow and ice has become a daily companion that
is turning a long-stable world upside down. Global warming and
pollution are increasing in the Arctic north of Canada “at a much
faster rate than even the most pessimistic predictions of a decade
ago” (Bourrie 1998). Inland Arctic areas are warming by 1.5⬚C per
decade (“Conservation” 1999). In 1999 overall Canadian tempera-
tures were also above average by 1.5⬚C, the third-warmest year of
the past half-century. The 1990s were the warmest decade on rec-
ord in Canada, followed by the 1980s. Canada’s warmest year of
record was 1998.
Arctic Network reports that weather records from Siberia, Alaska,
and northwestern Canada indicate a rise in mean temperature of
approximately 1⬚C each decade for the last thirty years. The surface
area of sea ice has been declining at a rate of 2.8 percent per decade
for twenty years, a process that has accelerated since 1987 to a
decadal rate of 4.5 percent. Many animals that are dietary staples
of indigenous communities are ecologically dependent on the sea
ice; smaller ice coverage means smaller habitats and smaller sus-
tainable human harvests.
Dwane Wilkin, a reporter for the Nunatsiaq News, in Iqaluit, sum-
marized the consequences of global warming for that area: “The
good news is that sailing through the Northwest Passage will finally
be a cinch. The bad news? Well, global warming will probably drive
musk oxen, polar bears and Peary caribou into extinction. And other
species—including humans—will face declining food sources.”
58 The Dirty Dozen
(Wilkin 1997). Warmer average temperatures north of 60 degrees

north latitude may mean that the Arctic Ocean will become ice-free
much of the year, imperiling populations of walrus and seal that
feed on creatures for whom ice means food and life.
“Our ice is getting thinner and going out. This year, we had very
thin ice and it went out real fast,” said Inuit elder Alexander Akeya.
“It’s getting more windy, and we have to hunt farther out than we
used to before” (Braem 1997). Elder Jimmy Toolie had a similar ob-
servation: “Today it has changed, the ice moves all the time, and
goes away quicker. We used to have it to mid-June. This year it went
out in mid-May. Even in the whaling time, it seemed it went away
so quick,” Toolie said (Braem 1997). Another Inuit, Joe Noongwook,
agreed: “This is true. We used to have huge icebergs come first be-
fore the young ice formed. We used to have thick ice from here to
the [Russian] mainland to the north, but now there is thin ice. There
is no hardpack ice” (Braem 1997). Several other Inuit said that the
ice has been thinning especially during the last twenty years.
“Those of us who are dependent on Arctic resources know global
warming is occurring,” said Caleb Pungowiyi, a Yup’ik Inuit elder.
“It is affecting us, and the impacts in some cases are quite severe”
(“Global Warming” 1998). Pungowiyi lives in Savoonga, a village of
about 500 people, near Nome, Alaska. The people of Savoonga make
their livings mainly from the sea, harvesting seals, walrus, polar
bear, whales, salmon, trout, whitefish, and other marine species.
Yup’ik elders in the small coastal Alaskan village of Kipnuk believe
the village is sinking because of warming permafrost. Buildings in
the village show signs of an unstable ground surface, signs that are
consistent with those of an area that sits above thawing land. In
Kotzebue, Alaska, the hospital has been relocated because it was
sinking into the ground.
Rising seas and coastal erosion directly threaten Tuktoyaktuk, a
Dene and Inuit community at the edge of the Arctic Ocean. Ice that
once protected the coast has receded out to sea. Extensive erosion
washed away the school and has forced the village to relocate many
other structures.
The bay on which Iqaluit sits is named for Martin Frobisher, an
early explorer who sought a northwest passage from Europe to Asia.
With the polar ice cap in the Canadian Arctic melting, the fabled
Northwest Passage is now opening. Commercial shippers are eyeing
the prospect of cutting more than four thousand miles off their
usual trip through the Panama Canal, bringing one more finger of
the industrial south to the Arctic.
In the Canadian Inuit town of Inuvik, ninety miles south of the
Arctic Ocean, the temperature rose to 91⬚F on June 18, 1999, a type
of weather unknown to living memory in the area. “We were down
to our T-shirts and hoping for a breeze,” said Richard Binder, fifty,
a local whaler and hunter. Along the Mackenzie River, according to
Binder, “Hillsides have moved even though you’ve got trees on them.
The thaw is going deeper because of the higher temperatures and
longer periods of exposure.” In some places near Binder’s village,
the thawing earth has exposed ancestral graves, and remains have
needed to be reburied (Sudetic 1999, 106). Some hunters say that
seals have moved farther north, killer whales are eating sea otters,
and beaver are proliferating, none of which would happen if rivers
and ponds were freezing to usual depths.
LAND OF MELTING ICE AND BURNING

TUNDRA
As tundra and permafrost thaws, it releases stored carbon dioxide
and methane, which further raises the atmosphere’s level of green-
house gases. During Alaska’s unusually warm, dry winter of 2000–
2001, the snowless tundra caught fire along Norton Sound, a
possible precursor of larger smoldering fires that could further ac-
celerate global warming. There is a palatable fear among climate
scientists that such “biotic feedbacks” in the oceans and on lands
could release large amounts of carbon dioxide and methane that are
now stored in earth.
Further evidence that the Earth’s frozen reaches already are re-
leasing additional greenhouse gases into the air has been provided
by M. L. Goulden and colleagues (1998), who studied boreal forests,
finding evidence that “provides clear evidence that carbon dioxide
locked into permafrost several hundred to seven thousand years
ago is now being given off to the atmosphere as warming climate
melts the permafrost” (Goulden et al. 1998, 214). These researchers
investigated black spruce forest and found that carbon dioxide was
being emitted into the atmosphere from well beneath the biologically
active layer containing moss and tree roots (Goulden et al., 1998).
The same is true in many cases for methane. According to Davis
(2001), this “relict” carbon dioxide
60 The Dirty Dozen
represents a massive source since it is estimated that the carbon dioxide

contained in the seasonally and perennially frozen soils of boreal forests is
200 to 500 billion metric tons, enough if all released to increase the atmo-
sphere’s concentration of carbon dioxide by 50 percent. Hence, it is possible
that the release of carbon dioxide from melting permafrost during warming,
or locking it into newly frozen soil during cooling, may accelerate climate
change. (Davis 2001, 270)
Coastal hunters above the Arctic Circle in Alaska say they are
definitely seeing a trend: The ice regularly comes a month later than
it did twenty years ago, and roughly two months later than thirty
years ago. Ice also breaks up earlier than previously, and so hunting
seasons are becoming shorter.
“Sea ice is a pretty sensitive indicator,” said Gunter Weller, a pro-
fessor of geophysics at the University of Alaska at Fairbanks. “It
doesn’t take much [temperature change] to make a change in the
ice” (Kizzia 1998). Weller noted that researchers on the National Sci-
ence Foundation’s ice ship Sheba found the polar ice cap north of
Alaska to be considerably thinner than previous studies had indi-
cated. They couldn’t find an ice floe thick enough to anchor their
icebreaker safely. Lack of sea ice causes a feedback warming effect
because open ocean absorbs more of the sun’s energy than ice and
snow.
The environmental group Greenpeace and the Arctic Network, a
nonprofit conservation group in Alaska, have been interviewing in-
digenous people of the Arctic about the condition of the ice with
which they live every day. These anecdotal accounts support statis-
tics indicating that Alaska’s climate is warming more rapidly than
any other place on Earth from an increase in carbon dioxide and
other greenhouse gases in the atmosphere.
Hudson Bay could be ice-free by the middle of this century. “We’re
starting to warm up very, very fast,” said Peter Scott, scientific co-
ordinator of the Churchill [Manitoba] Northern Studies Center
(“Hudson Bay” 2001). Scott said that climate change is bringing
some species to the Arctic that have never been seen there before.
“We may get southern animals. We’re seeing a lot of moose now. . . .
We now have moose in Churchill, where 20 years ago moose virtu-
ally didn’t exist” (“Time to Act” 2001).
Steven Kooneeliusie and the other Inuit who hunt caribou, seal,
and other animals say the signs of a gradual increase in tempera-
tures are everywhere around them. “When I went hunting years ago,
I used to wear a full-length caribou skin coat, but now I just wear a
light parka. It is so hot these days my snowmobile often overheats,”
Kooneeliusie said in the small town of Pangnirtung, about a hun-
dred miles north of Iqaluit, astride the Arctic Circle (Ljunggren
2000).
Sustainable development minister Peter Kilabuk, based in Iqaluit,
grew up in Pangnirtung. “I know when I was probably eight or ten
[years of age] the ice wouldn’t go out until July, sometimes not until
the second week of July. But over the last few years we’ve seen the
ice go out as early as May,” he said. (Some years, such as 2001, the
ice melted, as in previous years, in late June). “To us, the effects are
real. Climate change is here and it’s a real cause for concern”
(Ljunggren 2000). Grizzly bears and wolverines have been moving
north, said François Rainville at Environment Canada’s office in
Iqaluit. “There are insects and birds which have not been seen here
before. There is an impact. People are seeing change,” he said. Last
year one Iqaluit woman reported seeing a robin (Ljunggren 2000).
Pangnirtung is the main gateway to Auyuittuq National Park—
“the land that never melts,” the most northerly national park in
North America. Established in 1972, the park covers 19,500 square
kilometers of deep mountain valleys, dramatic fjords, ancient gla-
ciers, and spiny peaks. Auyuittuq (pronounced “ow-you-ee-tuk”) is
famed for its enormous glaciers. Local people say that even these
glaciers are slowly melting. “The glaciers have receded over the last
10 years, and the ice is much worse,” hunter Solomon Nakoolak
said (Ljunggren 2000).
“If you look at weather patterns for the next 40 years, you’ll see a
significant warming in the Eastern Arctic, but mainly in the winter,”
said Brian Paruk, a meteorologist with Environment Canada’s Arc-
tic Weather Centre (George 2000b). He said the two main influences
on Arctic weather to date have been the “incredible retreat” of the
sea ice and the resulting increase in precipitation. More open water
produces more rain. As a result of the lower temperature of the open
water, summer temperatures have declined in many coastal areas
(particularly along the Davis Strait) as they have risen inland.
HUNGRY POLAR BEARS AND A DYING

SEA-ICE ECOLOGY
The polar bear is one of the most visible casualties of a deterio-
rating ice ecology in the Arctic. Polar bears find their food supply
62 The Dirty Dozen
shrinking with the melting sea ice even as their bodies acquire
higher levels of organochlorines with each generation. In the pre–
global warming days, polar bears had their own food sources and
usually went about their business without trying to swipe food from
humans. Beset by the melting of the ice that once supplied them
with protein, hungry polar bears are coming into contact with peo-
ple more frequently. In Churchill, Manitoba, bears waking from
their winter’s slumber have found Hudson’s Bay ice melted. Instead
of making their way onto the ice in search of food, the bears walk
along the coast until they get to Churchill, where they get in the way
of motor traffic and pillage the town dump. Churchill now has a
holding tank for wayward polar bears that is larger than its jail for
people (Krajick 2001; Linden 2000). Around the Arctic, polar bears
have been observed anxiously pacing the shorelines, waiting for the
food-bearing ice that arrives later and later.
Canadian Wildlife Service scientists reported that during Decem-
ber 1998 polar bears around Hudson Bay were 90 to 220 pounds
lighter than thirty years ago, apparently because earlier ice melting
has given them less time to feed on seal pups. When sea ice fails to
reach a particular area, the entire ecological cycle is disrupted.
When the ice melts, the polar bears can no longer use it to hunt for
ring seals, many of which also have died, having had no ice on which
to haul out.
During 1999 a hungry polar bear mother and a cub surprised
some picnickers just outside Pangnirtung. The bears were shot after
they could not be scared away. On another occasion, a school group
from Arctic Bay, on the Arctic Ocean at the northern tip of Baffin
Island, was camped outside town. The children were playing radios
and otherwise making too much noise to notice the polar bear that
entered their camp and stuck its head into the tent of the biology
teacher. Awakened by the uproar, the group’s guide, Simon Qam-
anariq, stumbled from his tent to find the bear between him and his
qamatiik, the sledge pulled by his snowmobile where he kept his
rifle. All there was at hand was a tea kettle, which Simon threw with
a clatter at the polar bear’s feet. While the bear was distracted,
Simon ran for his gun and got off a few rounds, sending the bear
running (Rauber n. d.).
AN ALASKAN VILLAGE ERODES INTO THE

ARCTIC OCEAN
Six hundred people in the Inuit village of Shishmaref, on the
Chukchi Sea, about sixty miles north of Nome, have been watching
their village erode into the sea. The permafrost that had reinforced
its coast is thawing. “We stand on the island’s edge and see the
remains of houses fallen into the sea,” wrote Anton Antonowicz of
the London Daily Mirror. “They are the homes of poor people. Half-
torn rooms with few luxuries. A few photographs, some abandoned
cooking pots. Some battered suitcases” (Antonowicz 2000, 8).
Percy Nayokpuk, a village elder, runs the local store, which now
perches dangerously close to the edge of the advancing sea. “When
I was a teenager, the beach stretched at least 50 yards further out,”
said Percy. “As each year passes, the sea’s approach seems faster
(Antonowicz 2000, 8). Five houses have washed into the sea; the
U.S. Army has moved or jacked up others. The villagers have been
told they will soon have to move.
Year by year, the hunting season, which depends on the arrival of
the ice, starts later and ends earlier. “Instead of dog mushing, we
have dog slushing,” said Clifford Weyiouanna, 58, a reindeer herder
near Shishmaref (Antonowicz 2000, 8). Villagers have been catching
fish, such as flounder, which are usually associated with warmer
water.
By the summer of 2001, the encroaching sea was threatening a
rusty fuel-tank facility holding 80,000 gallons of gasoline and stove
oil. “Several years ago,” observed Kim Murphy of the Los Angeles
Times, “The tanks were more than 300 feet from the edge of a sea-
side bluff. But years of retreating sea ice have sent storm waters
pounding, and today just 35 feet of fine sandy bluff stands between
the tanks and disaster” (Murphy 2001, A1). Seawater is lapping
near the town’s airport runway, its only long-distance connection
to the outside. At last count, five houses had been washed into the
sea. Several more are threatened. The town’s drinking-water supply
also has been inundated by the sea. The sea is eight feet from cut-
ting the town’s main road and threatens to wash the town dump
out to sea.
Shishmaref hunters are being forced to search up to two hundred
miles from town for walrus because of retreating ice. They also now
use boats to hunt seals that they used to track over ice. “This year
the ice was thinner, and most of the year at least part of the ice was
64 The Dirty Dozen
open. We don’t normally see open water in December,” said Edwin

Weyiouanna, an artist who has lived most of his life on the Chukchi
Sea (Murphy 2001, A1). In earlier years, the sea was more likely to
be frozen during much of the stormy winter season. With warming,
the erosive wind-whipped ocean corrodes Shishmaref’s waterfront.
The town’s residents have come to fear the full moon, with its un-
usually high tides.
Gunter Weller, director of the Center for Global Change and Arctic
System Research at the University of Alaska in Fairbanks, said
mean temperatures in the state have increased by 5⬚F in the sum-
mer and 10⬚F in the winter over the last thirty years. Moreover, the
Arctic ice field has shrunk by 40 percent to 50 percent over the last
few decades and has lost 10 percent of its thickness, studies show.
“These are pretty large signals, and they’ve had an effect on the
entire physical environment,” Weller said (Murphy 2001, A1).
Increasing coastal erosion isn’t limited to Shishmaref; it is now
general on the shores of the Bering Sea, as increasing storm surges
crush ice packs that retreat several weeks earlier than thirty years
ago. Sea-ice extent in the Arctic has decreased Arctic-wide by 0.35
percent per year since 1979. During the summer of 1998, record
reduction of sea-ice coverage was observed in the Beaufort and
Chukchi seas (Maslanik, Serreze, and Agnew 1999).
In Tuktoyaktuk, a town near the mouth of the Mackenzie River,
several buildings have been lost to erosion by the sea. In addition
to a reduction in Bering Sea ice cover, more precipitation is falling
in many areas of Alaska. During the fall of 1998, sea ice formed in
northern Alaska more than a month later than usual, postponing
the annual seal and walrus hunt.
Average temperatures at the mouth of the Mackenzie River were
9⬚F above long-term averages during 1998. Several decades ago,
miners in the area deposited toxic wastes in ponds that were ex-
pected to remain frozen (and the toxic materials sealed by the per-
mafrost). With warmer temperatures, some of these toxic dumps
may thaw and leak.
In Alaska, where roughly 80 percent of glaciers are receding, for-
ests of dead spruce surround Anchorage, a casualty of a spruce-
beetle epidemic caused at least in part by rising temperatures,
which accelerate the insect’s life cycle. Large patches of Alaskan
forests have been described as drowning and turning gray as thaw-
ing ground sinks under them. Trees and roadside utility poles,
destabilized by thawing, lean at crazy angles. The warming has con-

tributed a new phrase to the English language in Alaska—“the
drunken forest.”
The Sierra Club of Canada created a television commercial that
highlights the impact of global warming on the Arctic, including the
disastrous effect of receding sea ice on polar bear populations and
the hardship that increasing snowfall brings to the endangered
Peary caribou. “Our way of life is on the edge of extinction. Plants
and animals are dying,” said Rosemarie Kuptana, a former presi-
dent of the Inuit Circumpolar Conference, who was recruited to host
the thirty-second spot (George 2000b).
On Earth Day 2000 Inuit brought their accounts of dramatic
warming to urban audiences in southeastern Canada. Kuptana told
a press conference in Ottawa that experienced hunters have fallen
through unusually thin ice. Three men had recently died this way.
Never-before-seen species (including mosquitoes, robins, barn
swallows, beetles, and sand flies) have appeared on Banks Island,
in the Arctic Ocean about eight hundred miles northwest of Fair-
banks, Alaska. Growing numbers of Inuit are suffering allergies
from white-pine pollen that recently, for the first time, reached
Sachs Harbour, on western Banks Island, along the Beaufort Sea.
“If this rate of change continues, our lifestyle may forever change,
because our communities are sinking with melting permafrost and
our food sources are . . . more difficult to hunt,” said Kuptana (Duffy
2000, A13). Sachs Harbour itself is slowly sinking during the sum-
mer into a muddy mass of thawing permafrost. Born in an igloo,
Kuptana has been an Inuit weather watcher for much of her life (she
was forty-six years of age in 2000). Her job was to scan the morning
clouds and test the wind’s direction to help the hunters decide
whether to go out and what everyone should wear. Now she gathers
observations for international weather-monitoring organizations.
“What happens in the Arctic environment is what is in store for other
regions of the world,” said Kuptana (Duffy 2000).
“We can’t read the weather like we used to,” said Kuptana (Duffy
2000), who grew up in Sachs Harbour. She said that autumn freezes
now occur a month later than they used to; spring thaws come ear-
lier as well. Residents of Sachs Harbour still suffer through winters
that most people from lower latitudes would find chilling, with tem-
peratures of minus 40⬚F or lower. While such temperatures were
once commonplace, however, they now are rare.
66 The Dirty Dozen
“The permafrost is melting at an alarming rate,” said Kuptana

(Herbert 2000). Foundations of homes in Sachs Harbour have been
cracking and shifting. Kuptana expressed fear that the community
will soon slide into the Beaufort Sea because once-solid mud is now
thawing earlier and freezing later.
“What’s scary is the uncertainty,” she said. “We don’t know when
to travel on the ice and our food sources are getting further and
further away” (Herbert 2000). Tracking animals on receding ice and
mushy ground poses new problems for Inuit hunters, some of whom
have been reporting sunburns for the first time. “We have no other
sources of food, the people in my community are completely depen-
dent on hunting, trapping and fishing,” said Kuptana. “We have no
means of adapting to a different environmental reality, and that is
why our situation is so critical” (Herbert 2000).
At Sachs Harbour, sea ice is thinner and now drifts far away dur-
ing the summer, taking with it the seals and polar bears upon which
the village’s Inuit residents rely for food. Many young seals are
starving to death because prematurely melting sea ice separates
them from their mothers. In the winter the sea ice often is thin and
broken, making travel dangerous for even the most experienced
hunters. In the fall, storms have become more frequent and often
more severe, making boating difficult. Thunder and lightning have
been seen for the first time, arriving with another type of weather
that is new to the area—dousing summer rainstorms.
“When I was a child, I never heard thunder or saw lightning, but
in the last few years we’ve had thunder and lightning,” Kuptana
said. “The animals really don’t know what to do because they’ve
never experienced this kind of phenomenon” (“Thunder Storms”
2000). “We don’t know when to travel on the ice and our food sources
are getting further and further away,” says Kuptana. “Our way of
life is being permanently altered” (Knight 2000). Andy Carpenter of
Sachs Harbour observed that “Different kinds of birds are coming
up. There’s other species of fish that we’ve never gotten before, like
the pink salmon” (“Scientists Look” 2001).
During 1997 and 1998, a team of 160 scientists lived on the ice
of the Arctic Ocean, about 500 kilometers from the North Pole. Their
headquarters aboard the Canadian icebreaker Des Groseilliers was
converted into a floating laboratory. Biologist Harold Welch, a re-
searcher on the team, said a comparison with studies done thirty
years ago documents significant melting of the polar ice cap.
“With climate warming, we get a thinning of the arctic ice pack

and more open water, and a longer summer with less snow cover,
which allows more light to come in,” Welch said (Bourrie 1998). Sci-
entists reported that the ice pack has become so thin that the re-
search camp nearly was lost several times as the ice around it split
apart. “A couple of times, we saw haze in the atmosphere and the
sun appearing as a red ball because of forest fires and other fires in
Asia. But much more important, we see contaminants, pollution,
that comes from Eurasia, primarily,” Welch said (Bourrie 1998).
Greenpeace activists during 1997 gathered information about
global warming from Yup’ik and Inupiat Inuit. They embarked on
the organization’s 150-foot ship Arctic Sunrise, on a route north to
Barrow along Alaska’s Arctic coast. The activists reported that Sa-
voonga whalers brought home no whales in 1997 because of a quick
and early breakup of ice that forced them to come home earlier than
usual. Inuit said that for several years they have been routinely
catching fish heretofore not considered native to the Arctic, includ-
ing chum and pink and silver salmon. Like observers across the
Arctic, Inuit interviewed by Greenpeace said they had observed
birds that are new to higher latitudes, such as various types of swal-
lows, finches, and robins.
A Canadian government report, Responding to Global Climate
Change in Canada’s Arctic, released late in 1997, did its best to put
a positive spin on global warming in the Arctic. Reading closely,
however, one realizes that most of the benefits accrue to industrial
society’s incursion into the Arctic. The report noted that reduced ice
cover would aid offshore oil and gas production and extend the ship-
ping season. In the western Arctic, said the same report, “New ag-
ricultural opportunities would arise” (Wilkin 1997).
Most of global warming’s debits are accruing to the Inuit, the ani-
mals of the region, and the traditional relationship of the two. The
report expects that precipitation will increase as much as 25 per-
cent with the advent of rapidly rising temperatures during a cen-
tury. When the precipitation falls as snow and ice, caribou and other
grazing animals will have a harder time finding food during lean
winter months. The study anticipates that heavier snow cover will
lead to smaller, thinner animals that will be forced to go further
afield for food in winter. The same animals will be plagued by in-
creasing numbers of insects during warmer summers. Environ-
mental stresses during the next century could lead to “complete
68 The Dirty Dozen
reproductive failure of the caribou in a worst-case scenario” (George

2000a).
The Canadian study forecasts that winter temperatures in the
mainland of the Canadian Arctic will rise by 5 to 7⬚C within a cen-
tury, unless greenhouse-gas emissions are drastically curtailed
worldwide. Such temperatures would melt more than half the ex-
isting permafrost in the Canadian Arctic, according to the same re-
port. Some fear that as the ground heats up airport runways and
buildings could crack (Wilkin 1997).
Other impacts of global warming include “wildlife habitat destruc-
tion, melting permafrost which destabilizes northern homes, roads
and pipelines, large-scale coastal erosion, and insect outbreaks”
(Ralston 1996). The report suggests that an increase in the inci-
dence of forest fires in the area may be attributed to rising tem-
peratures (Ralston 1996). Forest fires are adding even more
greenhouse gases to the atmosphere.
THE ACCUMULATION OF MERCURY IN THE

ARCTIC
In addition to accumulation of persistent organic pollutants,
springtime also brings mercury-laced precipitation to the polar re-
gions. The mercury arrives in much the same manner as dioxins
and PCBs, via prevailing currents in the ocean and atmosphere.
Fossil-fuel combustion releases about 6,500 tons of mercury vapor
into the atmosphere every year (“Mercury” 2002). “In just five
months during the spring each year,” according to a report by the
Environment News Service (ENS), “The northernmost coast of
Alaska, a region that includes the Arctic National Wildlife Refuge,
receives more than double the amount of mercury that falls on the
northeastern United States in a year” (“Mercury” 2002). Similar pol-
lution also occurs each year in the Antarctic.
Two studies in the March 15, 2002, edition of Environmental Sci-
ence and Technology, a journal published by the American Chemi-
cal Society, presented new information about what some scientists
had begun to call the “mercury sunrise,” which was first reported
in the Arctic during 1998 (Ebinghaus et al. 2002; Lindberg et al.
2002). The first sunrise of spring initiates a series of chemical re-
actions that dump mercury out of the atmosphere into polar snow
pack, from which it is released into the food web during the brief
polar growing season.
Ralf Ebinghaus, an environmental chemist at the Institute for

Coastal Research in Geesthacht, Germany, gave a description of the
mercury sunrise at Germany’s Neumayer research station in Ant-
arctica based on measurements between January 2000 and Janu-
ary 2001. According to an ENS report, Steve Lindberg, a research
corporate fellow at the Oak Ridge National Laboratory in Tennessee,
“presented the first evidence of how this phenomenon leads to ele-
vated mercury accumulation in snow, as measured at the National
Oceanic and Atmospheric Administration’s Climate Monitoring and
Diagnostic Laboratory in Barrow, Alaska” (“Mercury” 2002).
A research team led by Lindberg wrote that
Our data from Barrow, Alaska, at 71 degrees north, show that rapid, pho-
tochemically driven oxidation of boundary-layer HgO [gaseous elemental
mercury] after polar sunrise, probably by reactive halogens, creates a rap-
idly depositing species of oxidized gaseous mercury in the remote Arctic
troposphere. . . . This mercury accumulates in the snow pack during polar
spring at an accelerated rate in a form that is bio-available to bacteria and
is released with snowmelt during the summer emergence of the Arctic eco-
system. Evidence suggests that this is a recent phenomenon that may be
occurring throughout the earth’s polar regions.” (Lindberg et al., 2002,
1245)
The ENS report described findings of the Lindberg team, which

may help explain why mercury levels in Arctic seabirds, seals, and
beluga whales have increased over the last twenty years, even as
global atmospheric emissions of mercury have declined (“Mercury”
2002). The mercury sunrise is said by the scientists to depend on
ultraviolet light, open water, and active sea ice, all of which have
been increasing in polar regions during the last few decades. Ac-
cording to ENS, the Barrow data indicates that the polar sunrise
triggers a series of chemical reactions that convert elemental mer-
cury vapor into a soluble form of oxidized gaseous mercury that
accumulates in the polar snow pack (“Mercury” 2002). Ebinghaus
and Lindberg estimated that between 50 and 300 tons of mercury
were being dumped from the atmosphere into these polar environ-
ments each year by the year 2001.
STRATOSPHERIC OZONE DEPLETION IN THE

ARCTIC
Along with toxic pollutants and accelerating global warming, the
Inuit (and the Arctic ecosystem generally) are facing another im-
70 The Dirty Dozen
ported threat from the industrial south. Stratospheric ozone deple-

tion in northern latitudes and resulting increases in ultraviolet (UV)
radiation have increased markedly during the past decade, with
some sectors of the Arctic experiencing a 40 to 60 percent increase
in UV radiation (Taalas et al. 1996, 1997).
The National Science Foundation maintains a polar UV monitor-
ing Network, which has observed
In the last few decades, particularly in the 1990s, anthropogenic influences

on the natural ozone layer have resulted in severe ozone depletion in polar
regions. . . . During March 1997, stratospheric ozone in the Arctic reached
all-time lows with losses due to halogen-related chemistry rivaling the Ant-
arctic losses observed since the infamous “ozone hole” was discovered in
1985. Three-dimensional, coupled physical-chemical models indicate that
depletion of stratospheric ozone in the Arctic will increase in the future as
climate change cools the stratosphere and stabilizes the polar vortex during
the period when stratospheric chlorine and bromine from human-made hal-
ogen compounds will remain high for the next 20 to 30 years. (Bodhaine,
Dutton, and Tatusko 2001)
The same report continued “It is during the spring, when ozone de-
pletion is greatest, that biological systems are most susceptible to
UV damage: natural protective measures, such as pigmentation and
thickening of leaves, have not had time to develop, and fish larvae
are most exposed” (Bodhaine et al., 2001).
During the 1990s, the ozone column over the Antarctic failed to
heal as projected after the production of ozone-destroying chlorine
compounds was banned under the Montreal Protocol. According to
scientific analysis developing early in the twenty-first century, the
warming of the near-surface atmosphere (the lower troposphere) is
related to the cooling of the stratosphere, which drives ozone deple-
tion at that level. Increases in carbon dioxide and other greenhouse
gases near the Earth’s surface acts as a blanket, trapping the heat.
By 1998 the Antarctic ozone hole reached a new record size roughly
the size of the continental United States. A year later, it was roughly
the size of North America. The area of severely depleted ozone sta-
bilized during the next few years.
Steve Hipskind, atmospheric and chemistry dynamics branch
chief at NASA’s Ames Research Center, Moffett Field, California, has
been quoted as saying that chlorine atoms must use clouds as a
platform to destroy stratospheric ozone (“Arctic Region” 2000, 4).
Clouds form more frequently in the stratosphere at low tempera-
tures, most notably below minus 107⬚F. Ice crystals, which form as
part of polar stratospheric clouds, assist the chemical process by
which ozone is destroyed. During the winter of 1999–2000, tem-
peratures in the stratosphere over the Arctic were recorded as low
as minus 118⬚F (the lowest on record), forming the necessary clouds
to allow accelerated ozone depletion.
As temperatures fall in the Arctic stratosphere, the ozone column
has been depleted there as well. During April 2000 scientists from
the United States and Europe said that more than 60 percent of the
Arctic ozone layer about eleven miles above the Earth had vanished
during the winter because of record stratospheric cold and contin-
ued pollution—one of the most substantial ozone losses ever re-
corded there. Evidence is accumulating that indicates that ozone
depletion will continue to be a problem in the Arctic until the in-
dustrialized world substantially reduces its consumption of fossil
fuels. Even then, it will take about thirty to fifty years for various
feedback loops to reverse the rapid rise in near-surface tempera-
tures. Only after that will the thermal imbalance between the lower
and upper atmosphere correct itself, allowing the ozone shield to
restore itself. In the meantime, the survival of the Inuit, the polar
bears, and the rest of the Arctic ecosystem hang in the balance.
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3
CFCs, Global Warming, and
Ozone Depletion
Why has stratospheric ozone depletion over the Arctic and Antarctic
accelerated despite a decade-old ban on ozone-destroying chloro-
fluorocarbons (CFCs)? Why did the Antarctic ozone “hole” expand
during the year 2000 to an area the size of North America? Why has
ozone depletion also been increasing over the Arctic? Why are ozone
warnings being issued in Punta Arenas, Chile, and Ushuaia,
Argentina?
Part of the answer to this riddle appears to be rising levels of
greenhouse gases (carbon dioxide, methane, and others) near the
surface of the Earth. In an act of atmospheric irony, warming near
the surface of the Earth causes the ozone-bearing stratosphere to
cool significantly. The atmosphere’s existing cargo of CFCs (with a
lifetime of up to a century) consume more ozone the colder it gets.
An increasing level of carbon dioxide near the Earth’s surface “acts
as a blanket,” said NASA research scientist Katja Drdla. “It is trap-
ping the heat. If the heat stays near the surface, it is not getting up
to these higher levels” (Borenstein 2000).
Thus, until humanity reduces its emissions of greenhouse gases,
ozone depletion will remain a problem long after production of CFCs
has ceased. By the year 2001, the ozone-depleted area over Antarc-
tica grew, at its maximum extent, to an area the size of Africa. While
the polar reaches of the Earth have been suffering the most dra-
matic declines in ozone density, ozone levels over most of the Earth
have declined roughly 15 percent since the middle 1980s. The CFC
family of synthetic chemicals do more than destroy stratospheric
ozone. They also act as greenhouse gases, with several thousand
times the per-molecule greenhouse potential of carbon dioxide.
78 The Dirty Dozen
As levels of greenhouse gases rise, cooling of the middle and upper

atmosphere is expected to continue, with attendant consequences
for ozone depletion. Guy P. Brasseur and colleagues (2000) modeled
the response of the middle atmosphere to a doubling of carbon di-
oxide levels near the surface. Their models indicate that “A cooling
of about 8⬚Kelvin is predicted at 50 kilometers during summer.
During winter, the temperature is reduced up to 14⬚K. at 60 km. in
the polar region” (16). Increasing levels of methane, also a green-
house gas, enhance this effect. In addition to its properties as a
greenhouse gas, “methane oxidation leads to higher water and OH
concentrations in the stratosphere and mesosphere, and hence to
less ozone at these altitudes” (Brasseur et al. 2000, 16).
Why does anyone need to be worried if stratospheric ozone levels
decline? The major human motivation for concern is ozone’s role in
shielding flesh and blood residing on the surface from several fre-
quencies of ultraviolet radiation. One of these, ultraviolet B, is en-
ergetic enough to break the bonds of DNA molecules, the molecular
carriers of our genetic coding. While plants and animals are gen-
erally able to repair damaged DNA, on occasion damaged DNA mol-
ecules can continue to replicate, leading to dangerous forms of
basal, squamous, and melanoma skin cancers in humans.
The probability that DNA can be damaged by ultraviolet radiation
varies with wavelength, shorter wavelengths being the most dan-
gerous. “Fortunately,” writes one observer, “at the wavelengths that
easily damage DNA, ozone strongly absorbs ultraviolet radiation
and, at the longer wavelengths where ozone absorbs weakly, DNA
damage is unlikely. But given a 10-percent decrease in ozone in the
atmosphere, the amount of DNA-damaging ultraviolet radiation
would be expected to increase by about 22 percent” (Newman 1998).
A BRIEF HISTORY OF CFCS

CFCs initially raised no environmental questions when they were
first marketed by DuPont Chemical during the 1930s under the
trade name Freon威. Freon was introduced at a time when such
questions usually were not asked. At about the same time, asbestos
was being proposed as a high-fashion material for clothing, and ra-
dioactive radium was being built into timepieces so that they would
glow in the dark.
CFCs were first manufactured in 1930, a year after PCBs were
created. They were invented by Thomas Midgely, a chemist working
CFCs, Global Warming, and Ozone Depletion 79
for the Chevron Corporation. Their main use was as a propellant in

spray cans and fire extinguishers. They also came to be used widely
in compressors because, like PCBs, CFCs were useful for their sta-
bility. Before their effect on the ozone shield was detected (during
the 1970s) CFCs were touted as nontoxic. Also like PCBs, CFCs
accumulated in the atmosphere for several decades before negative
ecological effects were suspected.
Several varieties of CFCs have been synthesized; the most often
used are usually referred to as “F-11” and “F-12.” By the 1970s,
about 800,000 tons a year of CFCs were being injected into the at-
mosphere (Van Emden and Peakall 1996, 32), and some scientists
began wondering what had become of them. The scientists found
that CFCs were working their way into the stratosphere twenty to
twenty-five miles above the Earth’s surface, where they were con-
suming the ozone shield that protects the surface from harmful ul-
traviolet radiation.
By the 1970s, manufacturers in the United States were produc-
ing 750 million pounds of CFCs a year and finding all sorts of uses
for them, for example, as propellants in aerosol sprays; as solvents
to clean silicon chips; as home, office, and automobile air condi-
tioning refrigerants; and as blowing agents in the manufacture of
polystyrene cups, egg cartons, and containers for fast food. They
were amazingly useful, cheap to manufacture, nontoxic, and non-
flammable.
During June 1974 chemists Sherwood Rowland and Mario Molina
reported in Nature that CFCs were working into the stratosphere
and depleting the ozone column. Their research led to a cessation
of CFC manufacture by Du Pont, and a Nobel Prize in chemistry for
Rowland and Molina in 1995. The work of Rowland and Molina was
theoretical (Rowland and Molina 1974). Within a few years, their
theories were confirmed as scientists discovered, during the early
1980s, that CFCs were, in fact, rapidly thinning the ozone layer over
the Antarctic.
Stratospheric abundance of chlorine from human sources began
to increase rapidly shortly after World War II; by the year 1998, the
stratosphere contained roughly six times the natural background
amount provided by methyl chlorine emitted by the oceans (Crutzen
2001, 5).
At this point, opponents of CFC manufacture found themselves
facing a $28-billion-a-year industry. By the time their legal manu-
80 The Dirty Dozen
facture was banned internationally, CFCs had been used in roughly

90 million U.S. car and truck air conditioners, 100 million refrig-
erators, 30 million freezers, and 45 million air conditioners in
homes and other buildings.
AN OZONE “HOLE” IS DISCOVERED

During 1985 a team of scientists working with the British Ant-
arctic Survey reported a startling decline in “column ozone values”
above an observation station near Halley Bay, Antarctica (Farman,
Gardiner, and Shanklin 1985). Ozone densities had been declining
slowly over the Antarctic since 1977. The size of the decline in 1985
was a shocking surprise, however, because theorists had expected
stratospheric ozone levels to fall relatively evenly over the entire
Earth. Rowland and Molina (1974) had expected a largely uniform
worldwide decline of 1 to 5 percent. The seasonal variability of the
decline was another surprise, because existing theoretical models
made no allowance for it. Ozone values over Antarctica declined rap-
idly just as the sun was rising after the winter season.
During the middle 1980s, the cause of dramatic declines in ozone
density over the Antarctic was open to debate. Some scientists sus-
pected variability in the sun’s radiational output, and others sus-
pected changes in atmospheric circulation. A growing minority
began to suspect CFCs. These chemicals were not proven suspects
when, in 1987, a majority of the world’s national governments
signed the Montreal Protocol to eliminate CFCs.
Definite proof of CFCs’ role in ozone depletion arrived shortly
thereafter. J. G. Anderson, W. H. Brune, and M. H. Profitt (1989)
implicated the chemistry of chlorine and explained the chain of
chemical reactions (later broadened to bromides as a bit player)—
the “smoking gun”—that explained why ozone depletion was so
sharp and why it was limited to specific geographic areas at a spe-
cific time of the year. The temperature of the stratosphere later came
to be understood as a key ingredient in the mix—the colder the
stratosphere, the more active the chlorine chemistry that devours
ozone. By the year 2000, according to Maureen Christie (2001),
ozone depletion was “significantly affecting ozone levels throughout
the Southern Hemisphere” (86).
When the Montreal Protocol was signed, the best science available
was indicating that without remedial action the ozone destruction
rate would increase roughly 8 to 17 percent per year (a figure cal-

culated for the early 1990s); by about 1992, it was projected that
anthropogenic ozone destruction would rise to thirty-six times the
natural rate (Crutzen 2001, 7).
Matthew Stein, writing in When Technology Fails, describes how
chlorine atoms come to destroy stratospheric ozone:
CFCs are normally very stable, lasting 50 to 100 years before finally break-
ing down. CFCs are lighter than air and slowly migrate into the upper at-
mosphere, where high-energy rays from the sun blow them apart, liberating
a chlorine atom into the ozone layer. Each free atom of chlorine acts as a
catalyst, breaking up thousands of ozone molecules before finally reacting
with something else, which removes it from circulation. (Stein 2000, 17)
In the stratosphere, CFCs release reactive chlorine and bromine

that destroy ozone. The destruction is catalytic, as each chlorine or
bromine radical destroys thousands of ozone molecules. Stein also
pointed out that “In addition to CFCs, each new launch of America’s
Space Shuttle delivers tons of chlorine molecules from spent rocket
fuel directly to the upper atmosphere, where they eat away at the
planet’s ozone shield” (Stein 2000, 17).
The decline of stratospheric ozone is striking when viewed on a
graph with any sense of historical proportion. As little as a decade
or two will do. Until the 1990s, in the Arctic, springtime ozone levels
ranged around 500 Dobson units. By the year 2001 they were av-
eraging 200 to 300; in the Antarctic, in the days before the “ozone
hole” (about 1980) Dobson-unit values ranged from about 250 to
350; by the year 2000, they ranged from 100 to 200. Scientists usu-
ally call an area of the stratosphere ozone-depleted when its D.U.
level falls below roughly 200.
Measurements of stratospheric ozone above Arrival Heights, near
Scott Base in Antarctica, reached the lowest level ever recorded, 124
Dobson units, on September 30, 2000. The Antarctic ozone “hole”
formed earlier and endured longer during September and October
of 2000 than ever before. Figures from NASA satellite measure-
ments showed that the hole covered an area of approximately 29
million square kilometers in early September, exceeding the previ-
ous record from 1998. The record size persisted for several days.
Ozone levels fell below 100 D.U. for the first time in some areas. The
area cold enough to materially enhance ozone depletion also grew
to 10 to 20 percent more surface area than any previous year. By
82 The Dirty Dozen
the year 2000 the ozone-depleted zone was coming closer to New
Zealand, where usual springtime ozone levels average about 350
D.U. During spring 2000, ozone levels went as low as 260 D.U.
The atmosphere’s cargo of CFC’s did not dissipate immediately,
of course. Infrastructure using CFCs was replaced gradually, over
several years; CFCs also enter the atmosphere in a number of ways
not banned by the Montreal Protocol, some of them as prosaic (and
widespread) as frying food on a Teflon威-coated surface. Heated Tef-
lon also releases into the atmosphere small amounts of fluorocar-
bons, which are potent greenhouse gases.
Paul J. Crutzen asserts that problems with the stratospheric
ozone layer could have been much worse if chemists had developed
substances based on bromine, which is 100 times as dangerous for
ozone atom for atom as chlorine. “This brings up the nightmarish
thought that if the chemical industry had developed organobromine
compounds instead of the CFCs—or, alternatively, if chlorine chem-
istry had behaved more like that of bromine—then without any
preparedness, we would have faced a catastrophic ozone hole every-
where and in all seasons during the 1970s, probably before atmo-
spheric chemists had developed the necessary knowledge to identify
the problem” (Crutzen 2001, 10). Given the fact that no one seemed
overly worried about this problem before 1974, writes Crutzen, “We
have been extremely lucky.” This shows, he writes, “That we should
always be on our guard for the potential consequences of the release
of new products into the environment . . . for many years to come”
(Crutzen 2001, 10).
POLAR STRATOSPHERIC CLOUDS

The chlorine and bromine reactive forms are exacerbated by
chemical reactions that take place most efficiently on the surfaces
of cloud particles. Before the advent of fossil-fuel-forced global sur-
face warming (and stratospheric cooling) students of atmospheric
sciences were taught that clouds form in the stratosphere very
rarely, if at all. In the brave new world of atmospheric chemistry in
an era of whole-Earth pollution, however, polar stratospheric clouds
even have their own acronym: “PSCs.”
Mesospheric clouds form above the poles at altitudes of eighty-
two to eighty-six kilometers. They have been increasing in bright-
ness during the last four decades, and these changes may be linked
to anthropomorphic emissions of carbon dioxide and methane (“At-

mospheric Science” 2001). Gardner and colleagues (2001) report
measurements of the temperature, iron density, and altitude of po-
lar mesospheric clouds (PMCs) from an airplane. Results are re-
ported in Geophysical Research Letters (Gardner et al. 2001).
PSCs have been described as “Nacreous clouds resembling giant
abalone shells floating in the sky” (Tolbert and Toon, 2001, 61). Oc-
casional stratospheric clouds have been reported in Scandinavia for
a century, and Edward Wilson noted them during Robert Falcon
Scott’s 1901 Antarctic expedition. Sometimes the clouds shine with
green and orange shades at sunrise and sunset (Tolbert and Toon,
2001, 61).
PSCs remained largely an atmospheric curiosity until the discov-
ery of widespread ozone depletion over the Antarctic during the mid-
dle 1980s. Scientists surmised that the ozone loss was occurring in
the only place where the stratosphere is cold enough to produce
clouds. The clouds form during the springtime, when sunshine is
available, and their coverage seems related to rising levels of chlo-
rinated molecules, including CFCs and other synthetics. Observers
have noted “unprecedented concentrations of reactive chlorine in
conjunction with severe ozone loss” (Tolbert and Toon 2001, 61).
Ozone loss during the winter of 1999–2000 was exceptionally se-
vere, as record cold stratospheric temperatures produced abundant
polar stratospheric cloudiness.
THE EVOLUTIONARY NATURE OF THE SCIENCE

The relationship between CFCs, ozone depletion, and global
warming illustrates the evolutionary nature of the science of at-
mospheric chemistry. Industry invents the chemicals and puts
them to work, in the meantime changing nature’s chemistry in ways
that science detects and describes only decades later, often after
substantial ecological damage has been done.
A theoretical possibility that global warming could hasten ozone
depletion was suggested by mathematical model results reported in
the November 19, 1992, issue of Nature. J. Austin, N. Butchart, and
K. P. Shine (1992), climate modelers from the British Meteorological
Office and Reading University, ran a model simulating conditions
in the stratosphere in a world where atmospheric carbon dioxide
concentrations had been allowed to double, compared to preindus-
84 The Dirty Dozen
trial levels, which is the world in which we will be living in within

fifty years at present growth rates.
OZONE LOSS CONFIRMED IN THE ARCTIC

Scientists have been looking for reasons that the ozone shield has
failed to replenish itself after the international ban on production
of CFCs. During the middle 1990s, scientists began to model a re-
lationship between global warming and ozone depletion.
A team led by Drew Shindell, an atmospheric chemist at the NASA
Goddard Institute for Space Studies in New York City, created the
first atmospheric simulation to include ozone chemistry. The team
found that the greenhouse effect was responsible not only for heat-
ing the lower atmosphere, but also for cooling the upper atmo-
sphere. The cooling poses problems for ozone molecules, which are
most unstable at low temperatures. Based on the team’s model, the
buildup of greenhouse gases could chill the high atmosphere near
the poles by as much as 8⬚C to 10⬚C. The model predicted that max-
imum ozone loss would occur between the years 2010 and 2019
(Shindell, Rind, and Lonergan 1998, 589).
Stratospheric ozone loss in the Arctic was confirmed during the
winter of 1999–2000. An international group of researchers found
cumulative ozone losses of more than 60 percent at around 18 ki-
lometers (11 miles) above the Arctic between January and March
2000. “These are among the largest chemical losses at this altitude
observed during the last 10 years,” according to a statement of the
European Union, a main sponsor of the research (British Broad-
casting 2000). European Union spokeswoman Piia Huusela said the
report did not point to a hole in the ozone layer like the one that has
opened over the Antarctic, but a weakening of ozone content in the
stratosphere. Ozone amounts over the Arctic today are now said to
be 15 percent below the pre-1976 average. “This is not a hole in the
ozone layer,” said Huusela. “We are not even close to a hole, but it
is nevertheless alarming” (British Broadcasting 2000).
Jonathan Shanklin, of the British Antarctic Survey and one of the
three scientists credited with discovering the ozone hole over Ant-
arctica, warned in late October 2000, that global warming even-
tually threatens to create an ozone “hole” over the Arctic that
eventually may rival the Antarctic “hole” in size and severity. Shank-
lin told BBC Radio 4’s “Costing the Earth” program that Arctic ozone
depletion could affect the United Kingdom, bathing it in higher lev-

els of cancer-causing ultraviolet radiation. Shanklin said that the
buildup of greenhouse gases is trapping the sun’s heat, making the
Earth warmer, which has the effect of making the higher ozone layer
colder and increasing the catalytic action of ozone-killing chemicals
that concentrate over the poles (Nuttall 2000).
Shanklin, who, during 1985 first detected substantial strato-
spheric ozone depletion over the Antarctic with Joseph Farman and
Brian Gardiner of the British Antarctic Survey, said:
The atmosphere is changing, and one of the key changes is that the ozone
layer is getting colder. It’s getting colder because of the greenhouse gases
that are being liberated by all the emissions we have at the surface. And
when it gets colder, particularly during the winter, we can get clouds ac-
tually forming in the ozone layer, and these clouds are the key factor. Chem-
istry can take place on them that activates the chlorine and makes it very
much easier for it to destroy the ozone. We think that within the next 20
years we’re likely to see an ozone hole perhaps as big as the present one
over Antarctica, but over the North Pole. (Kirby 2000)
While most of the area covered by the Antarctic ozone hole is un-
inhabited by human beings, a similar Arctic hole would affect parts
of densely populated Europe, Asia, and North America. Following
the winter of 1999–2000’s record ozone loss in the Arctic, a Euro-
pean Space Agency satellite detected evidence that ozone levels
above Great Britain, Belgium, the Netherlands, and Scandinavia for
short periods “were nearly as low as those normally found in the
Antarctic” (Baker 2000, 38).
The World Meteorological Organization supported Shanklin’s
assessment:
Chemicals that result in ozone destruction are no longer increasing in the
stratosphere, as the international controls on ozone-depleting chemicals
continue to work. However, the continued general decrease of ozone in the
lower stratosphere and the global increase in greenhouse gases are now
believed to result in lower temperatures in the lower stratosphere. These
decreases in temperature could expand the period of intense ozone loss.
(Kirby 2000)
THE IMPORTANCE OF TEMPERATURE

SENSITIVITY
The extreme temperature sensitivity of these reactions has tre-
mendous consequences for Arctic ozone. A small cooling in the Arc-
86 The Dirty Dozen
tic stratosphere may provoke a much greater ozone loss. In some

cases, a 5⬚C decline in temperatures can multiply ozone loss ten
times.
Ozone depletion itself intensifies stratospheric cooling by reduc-
ing the upper atmosphere’s ability to absorb incoming ultraviolet
solar radiation. The amount of supercooled stratospheric territory
increased dramatically during the 1990s.
In 1998 the region of severely depleted ozone (“the ozone hole”)
over the Antarctic reached a record size roughly the size of the con-
tinental United States (it was three times that size two years later).
Some researchers have come to the conclusion that, as Richard A.
Kerr described in Science: “Unprecedented stratospheric cold is
driving the extreme ozone destruction. . . . Some of the high-altitude
chill . . . may be a counterintuitive effect of the accumulating green-
house gases that seem to be warming the lower atmosphere. The
colder the stratosphere, the greater the destruction of ozone by
CFCs” (Kerr 1998, 391).
“The chemical reactions responsible for stratospheric ozone de-
pletion are extremely sensitive to temperature,” Shindell said. He
continued: “Greenhouse gases warm the Earth’s surface but cool
the stratosphere radiatively, and therefore affect ozone depletion.”
By the decade 2010 to 2019, Shindell’s team expects ozone losses
in the Arctic to peak at two-thirds of the ozone column, or roughly
the same ozone loss observed in Antarctica by the early 1990s. “The
severity and duration of the Antarctic ozone hole are also expected
to increase because of greenhouse-gas-induced stratospheric cool-
ing over the coming decades,” Shindell has asserted (Shindell, Rind,
and Lonergan 1998, 589).
During the middle 1990s, scientists began to detect ozone deple-
tion in the Arctic after a decade of measuring accelerating ozone loss
over the Antarctic. By the year 2000, the ozone shield over the Arctic
had thinned to about half its previous density during March and
April. Ozone depletion over the Arctic reaches its height in late win-
ter and early spring, as the sun rises after the midwinter night. Solar
radiation triggers reactions between ozone in the stratosphere and
chemicals containing chlorine or bromine. These chemical reac-
tions occur most quickly on the surfaces of ice particles that form
stratospheric clouds at temperatures under minus 80⬚C (minus
107⬚F).
NEAR-SURFACE WARMING ABETS

STRATOSPHERIC COOLING
Space-based temperature measurements of the Earth’s lower
stratosphere, a layer of the atmosphere from about seventeen kilo-
meters to twenty-two kilometers (roughly ten to fourteen miles)
above the surface, indicate record cold at that level as record sur-
face warmth was reported during the 1990s. Roy Spencer of NASA
and John Christy of the University of Alabama at Huntsville and the
Global Hydrology and Climate Center obtained temperature mea-
surements of layers within the entire atmosphere of the Earth from
space, using microwave sensors aboard several polar-orbiting
weather satellites. They found that, despite significant short-lived
warming after the eruptions of El Chichón in Mexico in 1982 and
Mt. Pinatubo in the Philippines in 1991, the stratosphere has been
cooling steadily during the past fifteen years. During the winter of
1999–2000, temperatures in the stratosphere over the Arctic were
recorded at minus 118⬚F, the lowest on record.
As Dennis L. Hartmann and colleagues (2000) explained,
The pattern of climate trends during the past few decades is marked by
rapid cooling and ozone depletion in the polar lower stratosphere of both
hemispheres, coupled with an increasing strength of the wintertime west-
erly polar vortex and a poleward shift of the westerly wind belt at the Earth’s
surface. . . . [I]nternal dynamical feedbacks within the climate system . . .
can show a large response to rather modest external forcing. . . . Strong
synergistic interactions between stratospheric ozone depletion and green-
house warming are possible. These interactions may be responsible for the
pronounced changes in tropospheric and stratospheric climate observed
during the past few decades. If these trends continue, they could have im-
portant implications for the climate of the twenty-first century. (1412)
Ozone depletion has been measured only for a few decades, and
so researchers caution that they are not entirely certain that rapid
warming at the surface is not being caused by natural variations in
climate that are powerfully influenced by the interactions of oceans
and atmosphere. “However,” Hartmann and colleagues conclude, “It
seems quite likely that they are at least in part human-induced.”
Hartmann and associates also have raised the possibility that the
poleward shift in westerly winds may be accelerating melting of the
Arctic ice cap, part of what they contend may be a “transition of
88 The Dirty Dozen
the Arctic Ocean to an ice-free state during the twenty-first century”

(Hartmann et al., 2000, 1412). A continued northward shift in polar
westerly winds in winter also could portend additional warming over
the land masses of North America and Eurasia.
The connection between global warming, a cooling stratosphere,
and depletion of stratospheric ozone was confirmed in April 2000,
with release of a lengthy report by more than three hundred NASA
researchers as well as several European, Japanese, and Canadian
scientists. The report found that while ozone depletion may have
stabilized over the Antarctic, ozone levels north of the Arctic circle
were still falling, in large part because the stratosphere has cooled
as the troposphere has warmed. The ozone level over some parts of
the Arctic was 60 percent lower during the winter of 2000 than dur-
ing the winter of 1999.
In addition, scientists learned that, in coming years as winter
ends, the ozone-depleted atmosphere may tend to spread south-
ward over heavily populated areas of North America and Eurasia.
“The largest ultraviolet increases from all of this are predicted to be
in the mid-latitudes of the United States,” said University of Colo-
rado atmospheric scientist Brian Toon. “It affects us much more
than the Antarctic,” said Seth Borenstein (2000).
PROJECT SOLVE
NASA’s contribution to the Arctic ozone survey has been dubbed
SOLVE [SAGE (Stratospheric Aerosol and Gas Experiment) III
Ozone Loss and Validation Experiment]. SOLVE used satellites, air-
craft, balloons, and ground-based instruments between November
1999 and March 2000 to document changes in the Arctic ozone
shield. Scientists also gathered ozone-related data using the Rus-
sian Meteor-3 satellite, which was used to measure the vertical
structure of aerosols, ozone, water vapor, and other trace gases in
the Arctic upper troposphere and stratosphere. This information is
being used by more than two hundred scientists and support staff
from the United States, Canada, Europe, Russia, and Japan.
SOLVE and its Canadian, European, Russian, and Japanese
counterparts is the largest field measurement campaign devoted to
measure ozone amounts and changes in the Arctic upper atmo-
sphere. Researchers examined the processes that control ozone
levels at mid- to high latitudes during the Arctic winter between
November 1999 and March 2000. All this effort is being directed
toward understanding why the ozone column over the Arctic con-
tinues to deteriorate despite the banning of the main culprit in
stratospheric ozone loss, CFCs. Accelerating ozone loss has been
measured since the early 1990s in the Arctic.
The project’s main field office was established above the Arctic
Circle at the airport in Kiruna, Sweden. Arena Arctica, a large han-
gar especially built for research, housed the aircraft and many of
the project’s scientific instruments. Balloons were launched from
Esrange, a launch facility near Kiruna, where wintertime conditions
can be very severe, with temperatures falling below minus 50⬚F.
Kiruna is an optimal site for sampling Polar Stratospheric Clouds
because the stratosphere above Kiruna is usually quite cold, and
local meteorological conditions include mountain-forced waves,
which create even colder conditions, leading to PSC formation. Ki-
runa also is near the climatological average coldest region in the
Arctic. On average, the coldest point in the Arctic lower stratosphere
is located over Spitzbergen Island, a short flight from Kiruna.
Ross Salawitch, a research scientist at NASA’s Jet Propulsion
Laboratory in Pasadena, California, said that if the pattern of ex-
tended cold temperatures in the Arctic stratosphere continues,
ozone loss over the region could become “pretty disastrous” (Sci-
entists Report 2000, 3-A). Salawitch said that the new data has “re-
ally solidified our view” that the ozone layer is sensitive not only to
ozone-destroying chemicals but also to temperature (Stevens 2000,
A19).
“The temperature of the stratosphere is controlled by the weather
that will come up from the lower atmosphere,” said Paul Newman,
another scientist who is taking part in the Arctic ozone project. “If
we have a very active stratosphere we tend to have warm years;
when stratosphere weather is quiescent we have cold years” (Con-
nor 2000, 5). New research indicates that global warming will con-
tinue to cool the stratosphere, making ozone destruction more
prevalent even as the volume of CFCs in the stratosphere is slowly
reduced. “One year does not prove a case,” said Newman, who works
at NASA’s Goddard Space Flight Center in Greenbelt, Maryland.
“But we have seen quite a few years lately in which the stratosphere
has been colder than normal” (Connor 2000, 5).
“We do know that if the temperatures in the stratosphere are
lower, more clouds will form and persist, and these conditions will
90 The Dirty Dozen
lead to more ozone loss,” said Michelle Santee, an atmospheric sci-

entist at NASA’s Jet Propulsion Laboratory in Pasadena and coau-
thor of a study on the subject in the May 26, 2000, issue of Science
(McFarling 2000, A20). The anticipated increase in cloudiness over
the Arctic could itself become a factor in ozone depletion. The
clouds, formed from condensed nitric acid and water, tend to in-
crease snowfall, which accelerates depletion of stratospheric nitro-
gen. The nitrogen (which would have acted to stem some of the
ozone loss had it remained in the stratosphere) is carried to the
surface as snow.
PROJECTIONS OF STRATOSPHERIC OZONE

RECOVERY
Like all weather forecasts, the future of stratospheric ozone re-
covery is open to debate. One of the more optimistic forecasts states
that severe depletion in the Southern Hemisphere’s ozone layer will
start shrinking within a decade and should close completely within
the next fifty years. “Data from the Cape Grimm monitoring station
in Tasmania show that levels of CFCs in the lower atmosphere are
starting to decline for the first time since scientists from the British
Antarctic Survey discovered the ozone hole in 1985. A new mathe-
matical model, the most accurate yet devised, suggests that there
will be a similar decline in the stratosphere over the next decade,
leading to a recovery in levels of ozone” (Henderson 2000).
The report contains several caveats. “The dramatic recovery
could, however, be slowed by as much as 30 years by global warm-
ing or by severe volcanic eruptions, according to the meeting in Ar-
gentina of the Stratospheric Processes and Their Role in Climate
panel, which is a project of the World Climate Program. It will also
depend on continued efforts of the global community to keep ozone
emissions low. The hole could also grow slightly over the next five
years before recovery begins” (Henderson 2000).
Alan O’Neill, the director of the Centre for Global Atmospheric
Modelling, University of Reading, and chairman of the panel, said
that the news was a “triumph” for global cooperation (Henderson
2000). The success could be attributed to the 1987 Montreal Pro-
tocol, in which most governments pledged to reduce their use of
CFCs, he said.
Worldwide production of CFCs has declined sharply. The United
States has cut its annual output of ozone-depleting chemicals from
306,000 ozone-depletion potential tons (ODP tons) to 2,500 since

the Montreal Protocol was negotiated. The twelve nations that were
then members of the European Union have reduced their use from
301,000 to 4,300 ODP tons, while Japan has cut its output from
118,000 ODP tons to zero (Henderson 2000).
Sherwood Rowland of the University of California at Irvine, who
shared the 1995 Nobel Prize for Chemistry for his part in describing
the chemistry of stratospheric ozone depletion, believes that the ef-
fect of global warming on ozone depletion should be short-lived.
“The [ozone depletion] story is approaching closure, and that’s very
satisfying,” Rowland said (Schrope 2000, 627).
Drew Shindell agreed with Rowland, saying that even though sci-
entists are beginning to understand how global warming could de-
lay ozone-shield recovery, “The agreement to limit production [of
CFCs] has been an unqualified success. The science was listened
to, the policy-makers did something, and it actually worked”
(Schrope 2000, 627).
“ROCKS” IN THE STRATOSPHERE

During the year 2001, new scientific knowledge describing the
relationship of global warming and stratospheric ozone depletion
began to be published in leading journals. In Science, a team led by
A. Tabazadeh described a relationship between stratospheric cool-
ing, denitrification, and global warming. Tabazadeh and colleagues
(2001) wrote:
Homogeneous freezing of nitric acid hydrate particles can produce a polar

freezing belt in either hemisphere that can cause denitrification. . . . A 4
kelvin decrease in the temperature of the Arctic stratosphere due to an-
thropogenic and/or natural effects can trigger the occurrence of widespread
severe denitrification. Ozone loss is amplified in a denitrified stratosphere,
so the effects of falling temperatures in promoting denitrification must be
considered in assessment studies of ozone-recovery trends. (2591)
At about the same time, a team of atmospheric scientists led by

atmospheric chemist David W. Fahey (of the National Oceanic and
Atmospheric Administration’s office in Boulder, Colorado) discov-
ered large particles inside stratospheric clouds over the Arctic that
could delay the healing of the Earth’s protective ozone layer. The
team found large nitric-acid-containing particles that could delay
92 The Dirty Dozen
the recovery and make the ozone layers over both poles more vul-
nerable to climate change.
Fahey led a team of twenty-seven researchers that included sci-
entists from the National Oceanic and Atmospheric Administration
in Boulder, the University of Colorado, the National Center for At-
mospheric Research in Boulder, and the University of Denver. The
scientists described their findings in the February 9, 2001, edition
of the journal Science (Fahey et al. 2001). “It’s a major puzzle piece
in the process by which ozone comes to be destroyed,” Fahey said
of the discovery, which occurred during a January 2000 flight over
the Arctic in the ER-2, NASA’s version of the U-2 spy plane (Erickson
2001, 37-A). According to Richard Kerr, a machine on the aircraft
that was measuring nitrogen-containing gases “coughed out what
looked like disastrous noise” (Kerr 2001, 962). The “noise” turned
out to be very large particles (compared to other masses in Arctic
clouds) containing a form of nitric acid (HNO3), previously unknown
to science. The particles averaged 3,000 times the size of other at-
mospheric particles in the stratosphere.
Each winter in the stratosphere over the poles, water and nitric
acid condense to form clouds that unleash chlorine and bromine,
which degrade ozone. Later in the winter, nitrogen compounds help
shut down the destruction. Fahey’s team found previously un-
known nitric acid particles that remove nitrogen, allowing the de-
struction to continue. They nicknamed them “rocks” because they
are so much larger than any other type of particle in PSCs.
The “rocks” form during the polar winter, when stratospheric tem-
peratures are at their lowest. Cooling of the stratosphere compelled
by the retention of heat near the surface of the Earth may cause
more “rocks” to form, accelerating ozone depletion. “If it gets colder
and you get more ‘rocks,’ the depletion period is going to last longer.
The chlorine can continue to eat ozone,” said Paul Newman, an at-
mospheric physicist at NASA’s Goddard Space Flight Center in
Maryland (Erickson 2001, 37-A). “What [they] got is really outstand-
ing,” Newman said of the findings by Fahey’s team. “This mecha-
nism that we now understand really will help us be able to more
precisely predict what’s going to happen in the future.”
No one yet has even hazarded so much as a guess about how the
“rocks” form. These PSC particles remove nitrogen from the atmo-
sphere that would otherwise “tie up chlorine and bromine in inac-
tive, harmless forms” through denitrification (Kerr 2001, 963).
The “rocks” also “provide surfaces where chlorine and bromine can
be liberated from their inactive forms to enter their ozone-destroying
forms” (Kerr 2001, 963). In addition, the large size of the PSC
“rocks” causes them to fall more quickly than other particles, re-
moving even more nitrogen from the stratosphere. Through all these
mechanisms, according to Fahey and his colleagues, (2001, 1026)
the PSC “rocks” “have significant potential to denitrify the lower
stratosphere.”
Fahey and his colleagues (2001) concluded:
Arctic ozone abundances will remain vulnerable to increased winter/spring

loss in the coming decades as anthropogenic chlorine compounds are grad-
ually removed from the atmosphere, particularly if rising concentrations of
greenhouse gases induce cooling in the polar vortex and trends of increasing
water vapor continue in the lower stratosphere. Both effects increase the
extent of PSC formation and, thereby, denitrification and the lifetime of ac-
tive chlorine. The role of denitrification in these future scenarios is likely
quite important. (1030)
Fahey and his colleagues estimate that ozone depletion in the Arc-
tic stratosphere may not reach its peak until the year 2070, even
with a steady decline in CFC levels.
THE “FRIO BANDITOS”

Ozone-consuming CFCs continue to be used in older air condi-
tioners in the United States. Because manufacture of CFCs is illegal
in the United States, a flourishing smuggling trade has developed
from Mexico. Bert Ammons of Stuart, Florida, for example, pled
guilty to violating the Clean Air Act when he attempted to smuggle
ninety thirty-pound cylinders of CFC-12, also known by its trade
name, Freon, in false compartments on his forty-one-foot boat,
Sierra. According to Environmental Protection Agency officials, Am-
mons had planned to distribute $68,000 worth of smuggled CFCs
to auto repair shops around Fort Lauderdale. The crimes of which
Ammons was accused carry a maximum of five years in prison and
$250,000 in fines (Baker 2000, 34).
In Mexico and China (among other developing nations), CFC-12
can be bought for $1 or $2 a pound and resold in the United States
for $20 to $25 a pound. Why the huge domestic markup? It’s a sim-
ple matter of supply and demand (Baker 2000, 34). Millions of
pieces of equipment that use CFCs are still in service, including
94 The Dirty Dozen
automobiles built before 1994, air conditioners, and other refrig-

eration equipment.
Between 1994 and 1997, at least 6,367 tons of CFC-12 and 24
tons of CFC-113 (used as a fire suppressant) were smuggled across
the U.S. border. According to an unnamed official in the EPA’s Crim-
inal Enforcement Division, “Illegal CFCs rank close to cocaine as
some of the most profitable contraband coming across the U.S. bor-
der” (Baker 2000, 34). Smugglers of Freon over the Mexican border
have come to be called “frio banditos” (Baker 2000, 36).
By the late 1990s, CFC smuggling had become a multimillion dol-
lar business, big enough for the Justice Department and the Envi-
ronmental Protection Agency to make a priority of prosecuting it.
During January 2003, for example, a ring of CFC smugglers that
had collected more than $6 million in profits between 1996 and
1998 were sentenced. Barry Himes, the leader of the ring, was or-
dered to spend up to six and a half years in prison. Himes, who also
forfeited a $3 million mansion, a BMW sedan, and a three-carat
diamond ring, also was ordered to pay $1.8 million in restitution.
Coconspirator John Mucha was sentenced to up to four years in
prison and $1.2 million in restitution. Ten defendants were charged
as part of this particular smuggling operation. In all, by early 2003,
114 people had been charged with smuggling CFCs into the United
States.
SHOWDOWN OVER METHYL BROMIDE

Another threat to stratospheric ozone is methyl bromide, which
is used in the United States primarily by California strawberry and
Florida tomato growers. A showdown over use of this chemical has
been ongoing in Congress, where legislation introduced by Califor-
nia congressman Richard Pombo (the Methyl Bromide Fairness Act)
would push back the U.S. phase-out date of the chemical to 2015—
the year developing countries are required to stop production and
consumption of the chemical (Baker 2000, 34).
“Due to its acute toxicity,” one observer has written, “methyl bro-
mide is already banned in several countries, including the Nether-
lands and Canada. For years, environmentalists and health officials
in the U.S. (which uses 40 percent of the world’s methyl bromide)
have called for stricter regulation of this pesticide, especially in ag-
ricultural areas such as California’s Ventura County, where chil-
dren and farm workers are at risk. Since 1982, nearly 500
poisonings linked to methyl bromide have occurred in California,
19 of them fatal” (Baker 2000, 34).
Azadeh Tabazadeh, an atmospheric chemist at the NASA Ames
Research Center, Mountain View, California, said, “the bromide in
methyl bromine is a much better catalyst for ozone destruction than
chlorine.” She added: “And just because we’ve reduced the amount
of chlorine in the atmosphere doesn’t mean that the level of bromine
is also going down. That’s why compounds like methyl bromide need
to be regulated” (Baker 2000, 37). The U.S. EPA classifies methyl
bromide as a Class 1 ozone-depleting substance to be phased out
under the provisions of the Clear Air Act.
Unregulated emissions of methyl bromide have increased, while
manufacture of CFCs has all but ended in the United States. A re-
port of the United Nations Environmental Program suggests that
methyl bromide production and use may be the single most impor-
tant variable in ozone depletion during the next several decades.
EROSION OF THE ATMOSPHERE’S NATURAL

CLEANSERS
A sharp drop in atmospheric concentrations of hydroxyl radicals,
chemicals that naturally purge the air of contaminants, has been
detected by scientists. The biggest drop has been noted in the North-
ern Hemisphere, site of most of humanity’s industrial infrastruc-
ture, and now home to an aerosol mist that may be accelerating the
chemicals’ demise. Hydroxyls oxidize pollutants, making them sol-
uble in water so that they wash away as part of liquid precipitation.
These molecules’ continued decline could spread smog and ac-
celerate atmospheric accumulation of greenhouse gases, as the
Earth loses one of its principal defenses against several polluting
compounds, including carbon monoxide, methane, and sulfur di-
oxide. During the last twenty-two years concentrations of the mol-
ecule have decreased an average of 10 percent worldwide, the study
found (Wang and Prinn 1998). One of the study’s authors is Ronald
G. Prinn, chair of the Department of Earth, Atmospheric, and Plan-
etary Sciences at the Massachusetts Institute of Technology.
Hydroxyl radicals “are created as ultraviolet light knocks hydro-
gen atoms from water molecules in air in the presence of ozone, a
highly reactive form of oxygen” (Revkin 2001). The radicals vanish
96 The Dirty Dozen
almost as quickly as they are created, usually in less than a second,

as they react chemically with several air pollutants, including car-
bon monoxide, methane, and sulfur dioxide. One of many possible
influences, atmospheric scientists say, is an increase in aerosol
haze, a common by-product of fossil-fuel combustion, that could
block ultraviolet light and impede the reaction that creates the mol-
ecules (Revkin 2001). Hydroxyl radicals may purge more than half
the sulfur dioxide added to the air by industry, volcanoes, and other
sources.
Ralph J. Cicerone, an atmospheric chemist at the University of
California at Irvine, said about these new findings that “This is a
terrifically important question because hydroxyl radicals are the
central chemical in the lower atmosphere for processing every-
thing,” he said. “For 25 years, people have been struggling to mea-
sure [them]” (Revkin 2001).
Because hydroxyl radicals’ lives are so short, scientists often
must study them indirectly, usually by examining changes in con-
centrations of methyl chloroform, a long-lived solvent in the air that
can be neutralized only by the hydroxyl radicals. Methyl chloro-
form’s manufacture was banned during the 1990s because it also
contributes to the destruction of stratospheric ozone.
Stephen A. Montzka, a research chemist for the National Oceanic
and Atmospheric Administration, reflected on the fact that the sci-
entists are using proxy measurements of the radicals that may not
be reliable. However, he said that Prinn’s work has produced “the
best barometer of hydroxyl radicals that we have, but there are still
big potential sources of error” (Revkin 2001).
“This one molecule is very, very important. It is the critical clean-
ing chemical for the atmosphere,” said Prinn, who led a thirteen-
member research team for the study. “If this free-radical [molecule]
is decreasing, it could add to global warming” (Polakovic 2001, A1).
Losses of the chemical, a hydroxyl radical, “are slight so far and
are not currently cause for alarm” (Polakovic 2001, A1). “If this
change has happened, it is a slight change. It’s significant if it’s the
beginning of a trend. That would be a warning,” said Sherwood Row-
land, a chemist at the University of California at Irvine (Polakovic
2001, A1).
“We are seeing for the first time that the oxidizing capacity of the
atmosphere may have been reduced in recent years,” said Ray F.
Weiss, professor of geochemistry at the Scripps Institution of
Oceanography (Polakovic 2001, A1). These molecules also are es-

pecially efficient neutralizers of hydrocarbons from paints, solvents,
and petroleum that cause smog and cancer. About 18 million tons
of hydrocarbons are released into the atmosphere annually in the
United States (Polakovic 2001). “Eventually, the atmosphere will get
to the point where it will be taxed beyond its ability to clean itself,”
said Chris Cantrell, atmospheric chemist at the National Center for
Atmospheric Research in Colorado (Polakovic 2001, A1). Human
emissions of various pollutants may overwhelm the atmosphere’s
remaining defenses within fifty years, according to California Insti-
tute of Technology scientist John H. Seinfeld (Polakovic 2001, A-1).
Prinn and colleagues acknowledge a wide margin of error in their
data. They assert, more specifically, that “the actual loss of cleans-
ing molecules could be 24 percent greater than they have predicted,
or much less” (Polakovic 2001, A1). “Unless we cut the amount of
pollution we produce, we could end up facing a horrendous di-
lemma: Mend the ozone layer and suffocate in smog, or leave the
ozone layer damaged and let hydroxyl [radicals] keep cleaning up
our atmosphere. Either option is disastrous,” wrote Jeremy Webb,
editor of the New Scientist (Freeman 2001, 3).
The New Scientist painted a doomsday picture of the year 2050—
a world in which asthma has become the number-one killer of peo-
ple thirty years of age, “where Japan chokes in the sulfur dioxide
fumes from China, and where famine takes hold across Russia due
to crop failure” (Freeman 2001, 3). By 2070, this New Scientist re-
port “imagines that the fortunate few will be taking refuge in great
city domes, abandoning billions more to live outside amid the con-
tamination where life expectancy is reduced to 30 years” (Freeman
2001, 3).
GLOBAL WARMING, OZONE DEPLETION, AND

THE DEVASTATION OF THE BLUE WHALE
Global warming and ozone depletion interface in many ways.
Consider the impending demise of the blue whale, the largest ani-
mal ever to live on Earth. The blue whale is endangered because of
global warming as well as ozone depletion, according to the World
Wildlife Fund. Populations have fallen from an estimated 300,000
whales in 1900 (250,000 of them in waters around Antarctica) to
fewer than 5,000 by the year 2000. The blue whale’s main food
98 The Dirty Dozen
source, shrimp-like krill, are dying because of climate change. The

whales are going hungry after their populations had been reduced
by decades of aggressive whaling.
Krill feed on microscopic marine algae frozen in polar sea ice,
which are released each summer when the ice melts. The World
Wildlife Fund asserts that as the Earth’s temperatures have in-
creased in recent decades, sea ice has diminished enough to ma-
terially reduce krill populations. The WWF report also contends that
sharp reductions in stratospheric ozone density are allowing ultra-
violet radiation to cause DNA damage and excess mortality in krill.
Stuart Chapman, a whale specialist for WWF, said, “If this decline
continues . . . it could lead to the extinction of the Antarctic blue
whale” (Urquhart 2001, 7).
THE EVOLVING COMPLEXITY OF

STRATOSPHERIC OZONE CHEMISTRY
By 2002 most atmospheric chemists were recognizing that heal-
ing stratospheric ozone was not as simple as outlawing manufac-
ture of chemicals, such as CFCs, that increase levels of chlorine in
the upper atmosphere. A Canadian study released in early 2002
cast doubt on earlier optimistic prospects that stratospheric ozone
levels would steadily increase throughout the twenty-first century
as levels of chlorinated compounds declined. “The more we know,
the more we realize we don’t know,” said Jack McConnell, an at-
mospheric science professor at York University in Ontario, Canada
(Calamai 2002, A8). The Canadian study projected a decline in
stratospheric ozone levels over Canada throughout the century,
leading to a rise in some skin cancers of about 10 percent (Calamai
2002, A8).
The Canadian study cited new research by Australia’s national
scientific agency CSIRO that examined the relationship between
stratospheric ozone levels and two key greenhouse gases, nitrous
oxide and methane. Nitrous oxide, which remains in the atmo-
sphere about 120 years, comes from sources that are difficult to
control, such as agricultural soils and vehicle emissions, so a con-
tinued buildup in the atmosphere is almost certain. As it slowly
breaks down, nitrous oxide destroys ozone (Calamai 2002, A8).
According to an account in the Toronto Star by Peter Calamai,
A CSIRO computer model described in the journal Geophysical Research
Letters forecasts that this combination will keep levels of stratospheric
ozone depressed throughout this century, despite the global ban on the
chlorine chemicals responsible for the ozone holes over the North and South
poles. The most optimistic projection is that ozone levels at the end of the
century would be roughly where they are now—5 percent below those in
1980 when the problem began. The model also forecasts that reducing
methane emissions, as Toronto has done at landfill sites—actually makes
matters worse for protective ozone and could drive the levels in 2100 down
to 9 percent below 1980 levels. (Calamai 2002, A8)
Methane, which accelerates global warming, helps to protect

against ultraviolet radiation because it produces ozone as it breaks
down chemically. Current global climate change strategy focuses on
pushing down methane levels while letting nitrous oxide levels rise,
which probably will cause ozone levels to fall.
The complexity of ozone-depletion chemistry indicates the risks
inherent in any attempt to manipulate the atmosphere for one out-
come without regard for others. “You have to look at all these chem-
icals and see how they interact and evolve over time,” said Tom
McElroy, an ozone specialist with the Meteorological Service of
Canada (Calamai 2002, A8).
Yet another problem for stratospheric ozone may be wildfires and
slash-and-burn agriculture in the tropics, major factors in a dou-
bling of moisture content in the stratosphere during the last half of
the twentieth century. “In the stratosphere, there has been a cooling
trend that is now believed to be contributing to milder winters in
parts of the northern hemisphere,” said Steven Sherwood, assistant
professor of geology and geophysics at Yale University. “The cooling
is caused as much by the increased humidity as by carbon dioxide”
(“Biomass Burning” 2002). “Higher humidity also helps catalyze the
destruction of the ozone layer,” Sherwood wrote in a Science journal
article. “More aerosols lead to smaller ice crystals and more water
vapor entering the stratosphere” (Sherwood 2002, 1272).
Cooling in the stratosphere causes changes to the jet stream that
produce milder winters in North America and Europe. By contrast,
harsher winters result in the Arctic (“Biomass Burning” 2002).
Sherwood said that about half the increased humidity in the strato-
sphere has been attributed to methane oxidation. It was not known,
however, what has caused the remaining additional moisture. Sher-
wood said that “Aerosols are smoke from burning. They fluctuate
seasonally and geographically. Over decades there have been in-
creases linked to population growth” (“Biomass Burning” 2002).
100 The Dirty Dozen
”Volcanic aerosols have been linked by A. Tabazadeh and her col-

leagues to loss of ozone over the Arctic, especially in the springtime,
due to denitrification and chlorine activation. This is related to the
fact that volcanic eruptions produce “clouds that have greater sur-
face area than typical arctic polar stratospheric clouds” (Tabazadeh
et al., 2002, 2609). The authors state that “Chemical processing on
volcanic aerosols over a 10-kilometer altitude range could increase
the current levels of springtime column ozone loss up to 70 percent
independent of denitrification” (Tabazadeh et al., 2002, 2609). A
cooling of the lower stratosphere due to global warming near the
surface may aggravate this loss.
Unlike the Antarctic, where the stratosphere is consistently cold,
stratospheric “weather” in the Arctic varies greatly. The general
trend has been toward colder stratospheric temperatures in part
because of global warming near the surface. According to Tabaza-
deh and her colleagues, “Significant ozone loss in the Arctic occurs
only in cold winters, and volcanoes can substantially increase this
loss by enhancing the spatial scales over which ozone molecules can
get destroyed in the stratosphere” (Tabazadeh et al., 2002, 2609).
Because they increase the risk of ozone loss in the Arctic (in con-
junction with colder than usual winters) volcanic activity will need
to be monitored especially closely during the next thirty years,
“while anthropogenic chlorine levels are still sufficiently high (about
3 p.p.b.) to cause severe ozone depletion” (Tabazadeh et al., 2002,
2609). Models indicate that early rapid growth in the Antarctic
ozone “hole” in the early 1980s may have been influenced by a
higher than usual level of volcanic activity, according to Tabazadeh
and her colleagues.
According to an account by the Environment News Service, “Large
volcanic eruptions pump sulfur compounds into the Earth’s atmo-
sphere. These compounds form sulfuric acid clouds similar to polar
stratospheric clouds made of nitric acid and water. The clouds of
nitric acid and water form in the upper atmosphere during very cold
conditions and play a major part in the destruction of ozone over
Earth’s poles” (“Volcanic Eruptions” 2002).
After eruptions, volcanic sulfuric acid clouds would boost the
ozone-destroying power of polar stratospheric clouds, the research-
ers said. “Volcanic aerosols also can cause ozone destruction at
warmer temperatures than polar stratospheric clouds, and this
would expand the area of ozone destruction over more populated
areas,” Tabazadeh said. “Nearly one-third of the total ozone deple-

tion could be a result of volcanic aerosol effects at altitudes below
about 17 kilometers (11.5 miles),” the researchers wrote. “Climate
change combined with after-effects of large volcanic eruptions will
contribute to more ozone loss over both poles,” Tabazadeh con-
cluded. “This research proves that ozone recovery is more complex
than originally thought” (“Volcanic Eruptions” 2002).
The authors conclude that a period of higher than usual volcanic
activity coupled with colder than usual temperatures in the strato-
sphere could cause ozone levels there to fall to “values measured
inside the Antarctic ‘ozone hole.’” The researchers place the prob-
ability of such a combination of circumstances at about 15 percent
during the next thirty years—50 percent chance of a “cold” year
times 0.31 percent chance of major volcanic activity, or what they
call a “volcanic cloudy year” (Tabazadeh et al., 2002, 2612). “There-
fore,” they write, “It is possible for about five Arctic winters in the
next three decades to be cold and volcanic.”
“A ‘volcanic ozone hole’ is likely to occur over the Arctic within the
next 30 years,” said Azadeh Tabazadeh, lead author of the paper
and a scientist at NASA’s Ames Research Center. “If a period of high
volcanic activity coincides with a series of cold Arctic winters, then
a springtime Arctic ozone hole may reappear for a number of con-
secutive years, resembling the pattern seen in the Antarctic every
spring since the 1980s,” Tabazadeh added (Volcanic, 2002).
ENDURING CONCERNS
The synergies of climate change—such as the interstice of strato-
spheric ozone depletion and global warming—may compound the
effects of any single phenomenon. As the impending extinction of
the Blue Whale illustrates, the ecological toll of one anthropogenic
process may be compounded by the impact of another. For example,
rising levels of methane in the stratosphere could increase levels of
water vapor there, allowing, when temperatures are cold enough,
larger numbers of PSCs, and thus more ozone depletion.
All the while, as science has discovered new ways to describe
these synergies, climatologists have been sharing the disquieting
notion that small shifts in global temperature could lead to sudden
and abrupt climate changes. The history of atmospheric chemistry
during the last few decades has been one of surprises. The major
102 The Dirty Dozen
provocation of the ozone hole was chlorofluorocarbons. According

to Paul Crutzen, an atmospheric chemist working in Germany who
shared a Nobel Prize for detecting ozone depletion over Antarctica,
“Had chemists earlier in the century decided to use bromine instead
of chlorine to produce coolants, a mere quirk of chemistry—the
ozone hole would have been far larger, occurred all year and severely
affected life” (McFarling 2001, A1). “Avoiding that was just luck,” he
said, noting that no scientist had predicted the scope of ozone de-
pletion. “We missed something very important. There may be more
of these things around the corner” (McFarling 2001, A1).
During the fall of 2002, nature threw scientists studying strato-
spheric ozone loss a curve. The area of severely depleted ozone over
Antarctica shrunk and split into two pieces during September 2002.
In 2002, the depleted area was smaller than at any time since 1988,
a shrinkage that scientists attributed to warmer-than-usual tem-
peratures in the stratosphere caused by atmospheric agitation.
“The Southern Hemisphere’s stratosphere was unusually dis-
turbed this year,” said Craig Long, meteorologist at NOAA’s Climate
Prediction Center. The size of the ozone-depleted area shrunk to
roughly 15 million square kilometers from its record size of 24 mil-
lion during September 2001. In addition, “This breakdown [of the
ozone-depleted area] is occurring exceptionally early in the year,
about two months earlier than normal,” said Henk Eskes, a senior
scientist at the Royal Netherlands Meteorological Institute. “The
depth of the ozone hole this year also is unusually small, about half
that recorded in 2001” (“Antarctic Ozone” 2002). By 2002, the ozone
“hole” had grown as large as continental North America. Scientists
warned, however, that the rapid shrinkage of areas affected by
ozone depletion should not be taken as a pattern. Eskes said that
a possibility that one of the two remnants could strengthen and
form an expanded area of severe ozone depletion “cannot be ex-
cluded” (“Antarctic Ozone” 2002).
In Punta Arenas, a city of 125,000 in southernmost Chile, a “solar
stoplight” with four warning levels is used to warn people of ultra-
violet levels. Children are taught ozone safety in schools. People
wear 50-proof sunblock even on cloudy days. When the solar stop-
light is set at orange, the second-highest of four levels, people are
told not to expose themselves to the sun more than twenty-one min-
utes a day between noon and 3 P.M. When the solar stoplight is set
at red, most people stay indoors.
“It’s a new way of living,” said Lidia Amarales Osorno, the Chilean
Health Ministry’s regional director here. “You’ll see the solar stop-
light posted in supermarkets, offices and schools, and we even have
an Ozone Brigade to raise consciousness about this problem”
(Rohter 2002, A-4).
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4
The Chemical Industry, Nonwhite
Communities, and the Third World
The dangerous legacy of hazardous synthetic chemical wastes, con-

taminated manufacturing sites, and polluting industries has fallen
disproportionately on poor, nonwhite communities in the United
States and burdened them with neighboring hazardous waste sites,
incinerators, petrochemical plants, lead contamination, dirty air,
and contaminated drinking water.
The burden also has fallen on Third World countries that have
become havens for “gift waste,” stockpiles of dangerous, largely
useless toxic contaminants. This chapter comprises a number of
detailed local accounts, with extended reporting on malathion
spraying on the Rosebud Reservation in South Dakota to the toxic
landscape of Akwesasne, a Mohawk reservation that straddles the
border between the United States and Canada, and “Cancer Alley,”
Louisiana, with its ranks of petrochemical plants.
A 1983 U.S. General Accounting Office study revealed that 75
percent of off-site, commercial hazardous waste landfills in the
southeast United States are located within predominately African-
American communities. A 1987 study, “Toxic Waste and Race” by
the United Church of Christ Commission for Racial Justice (the first
national study to correlate waste facilities and demographic char-
acteristics), found that race was the most significant factor in de-
termining where waste facilities are located.
The study said that roughly 60 percent of African-Americans and
Latino Americans live in communities with uncontrolled toxic waste
sites, and that 15 million African-Americans live in communities
with at least one site. For example, the U.S. Army’s Pine Bluff Ar-
senal, which holds 12 percent of the U.S. chemical-weapons stock-
108 The Dirty Dozen
pile, is located just outside Pine Bluff, Arkansas, which is 53 percent

black. A proposed $200 million incinerator under construction in
Pine Bluff would be the nation’s second chemical-weapons incin-
erator. Nearly 30 percent of Pine Bluff’s residents earn less than a
poverty-level wage as defined by the 1990 U.S. Census.
A 1992 study by the National Law Journal, “Unequal Protection,”
uncovered significant disparities in the way the U.S. Environmental
Protection Agency (EPA) enforces laws (National Law 1992). The
study found abundant evidence of a racial divide when the U.S. gov-
ernment cleans up toxic waste sites and punishes polluters. White
communities see faster action, better results, and stiffer penalties
than communities where blacks, Latinos, and other minorities
make up most of the population. The handful of descriptions that
follow are only a small sampling of the hot spot situations in mi-
nority communities.
MALATHION AND THE ROSEBUD SIOUX IN

MISSION, SOUTH DAKOTA
The town of Mission, on the Rosebud Sioux reservation in South
Dakota, was sprayed routinely with malathion until at least the
middle 1990s. In 1995, the man who sprayed the town died of can-
cer, according to Joe Allen, editor of the Circle, a Native American
newspaper published in Minneapolis (Allen 1995).
The Circle published detailed accounts of Mission’s spraying and
the miseries it caused Native American residents there. The article
began by comparing the massive press coverage provoked in the
United States by the nerve gas sarin in a Tokyo subway with wide-
spread ignorance that a derivative of the same chemical, malathion,
was being sprayed liberally on a South Dakota Indian reservation.
People living at Rosebud described the peculiar hissing sound of
the spraying machine as it was driven on its rounds, spreading a
dirty gray fog along the reservation’s dirt roads. When local resi-
dents confronted the sprayers, they were told the reservation was
being treated for mosquitoes. Soon, everything in their homes
smelled of the chemical—clothes, unwrapped food, furniture, cur-
tains, and more.
One Rosebud resident, Jane Kirby, who was pregnant at the time,
was stricken with splitting headaches after spraying of her neigh-
borhood. She took no medication because of her pregnancy, but her
The Chemical Industry, Nonwhite Communities, and the Third World 109
husband, who also had headaches, took several doses of aspirin.

They were no help. The same night, the Kirbys’ daughter Gemma,
two years old, awoke at night breathing in raspy gasps.
The next morning, the Kirbys called Mission’s mayor, Jack Her-
man, and demanded an end to the spraying. Herman refused and
laughed in their faces. A physician’s assistant provided the Kirbys
with information on malathion; they were surprised to learn that
it had been developed by Nazi Germany as a possible nerve-gas
weapon. Four days after Mission’s mayor had laughed in her face,
Jane went into labor, as her husband became progressively dizzier,
weaker, and prone to muscle cramps. Within a few days, the Kirbys
learned that fourteen other people on their street were suffering
similar symptoms.
On July 9, 1992, a city crew appeared at the Kirbys’ door with a
notice that spraying would resume the next day. The spray crew’s
members pledged to avoid the couple and their one-day-old infant.
The Kirbys had asked that their area be spared the spraying be-
cause of the infant, but Mayor Herman again refused. He said the
machine spraying the malathion could not be shut down easily for
one home on a given street. Instead of enduring the spraying, the
Kirbys spent the next night at a friend’s mouse-infested cabin in the
nearby countryside. Back in town, all during the summer spraying
season, people complained of headaches and of waking in the night
gasping for breath.
During summer 1992, people at Rosebud also began to trade ac-
counts of illnesses associated with pesticide spraying, including an
account of a man in his twenties and his dog who lived in the tiny
community of White Horse, near Mission. Both were found dead in
their home after the house was sprayed for cockroaches by an ex-
terminator hired through the reservation housing authority.
During summer 1993, Anna Carol Thin Elk, fifty-one, of Mission,
was caught in a malathion spraying. She thought little of it and wore
the same clothes the next day without having taken a shower. By
noon that day, pain was spreading through Thin Elk’s wrists and
she experienced waves of chills. Severe pain spread through her
entire body during the next three days, until she was wracked by
fever and leg spasms. She also experienced acute difficulty breath-
ing. Thin Elk was taken to Rosebud Hospital, where she noticed,
while waiting, that three or four children in the room also were hav-
ing trouble breathing. The first question the doctor asked each of
110 The Dirty Dozen
their mothers was, Have you been near the area being sprayed for
mosquitoes? By the time a doctor saw Thin Elk an hour and a half
later, she was semiconscious and nearly asphyxiated. Thin Elk was
then taken by ambulance to Rapid City General Hospital, three
hours away, the closest medical facility possessing the proper anti-
dote for malathion poisoning.
Thin Elk was discharged from the hospital the next day. She had
no medical insurance, no spare clothes, and no way to get back to
Mission other than a ride that was offered to her that day. For a
week, Thin Elk struggled to keep working with severe fatigue and
dizziness, as her employers denied her sick leave. When Thin Elk
complained to Mayor Herman about how the pesticides affected her,
according to the Circle’s account, “I was told I should move out of
town if I didn’t like it” (Allen 1995, 10).
The Circle published several other, similar accounts of Mission
residents who became ill from the spraying, some of whom experi-
enced periods of near paralysis. In the meantime, Ed Einspar, who
had sprayed most of the malathion on Mission, died. One day,
shortly before he died, Einspar completed his spraying rounds with-
out wearing a gas mask. Shortly thereafter, he suffered a severe
gastrointestinal illness that aggravated his chronic asthma and em-
physema. Einspar’s niece, six-year-old Fianna White Hawk, suf-
fered a type of chronic pneumonia that has been attributed to
malathion exposure (Allen 1995).
Malathion was being sprayed in Mission despite the fact that the
chemical itself posed a much larger human-health risk to people
at Rosebud than to the mosquitoes it was being used to eradicate.
The area has no record of mosquito-borne disease, and so the in-
sects are more an irritant than a serious threat to human or ani-
mals’ health. Some Mission town officials were quoted in the Circle
article saying that AIDS could be spread by mosquitoes. No one
knows who told them that, or whether they believed it. The City
of Minneapolis decided in 1982 that malathion was little good
against mosquitoes, because its effects on them largely vanished
with the next substantial rainfall and egg-laying cycle. Salesmen of
malathion-contaminated sprays were using mosquito-phobia to sell
a dangerous product.
The malathion sprayed at Mission probably was given to the town
by the U.S. Department of Agriculture, which has, at various times,
had a policy of forwarding surplus pesticides to municipal govern-
ments. Malathion is especially dangerous to alcoholics, because the

liver of most alcoholics has been damaged beyond its ability to deal
with the pesticide, which then overwhelms the body. It is also nearly
as dangerous inhaled as absorbed through the skin. Roughly 75
percent of Rosebud’s population suffers from alcoholism, according
to Mission’s Little Hoop Lodge Treatment Center (Allen 1995).
AKWESASNE: LAND OF THE TOXIC TURTLES

For several centuries of human occupancy, the site the Mohawks
call Akwesasne was a natural wonderland: well watered; thickly for-
ested with white pine, oak, hickory, and ash; home to deer, elk, and
other game animals. The rich soil in the bottomlands of a valley into
which several rivers flowed allowed farming to flourish. The very
name that the Akwesasne Mohawks gave their territory about 1755
testifies to the bounty of the land. Akwesasne in the Mohawk lan-
guage means “Land Where the Partridge Drums,” after the distinct
sound that a male ruffed grouse makes during its courtship rituals.
Lying at the confluence of the Saint Lawrence, Saint Regis, Rac-
quette, Grass, and Salmon rivers, Akwesasne, until recent times,
also provided its human occupants with large runs of sturgeon,
bass, and walleye pike.
Within roughly half a century, this land of natural wonders has
become a place where one cannot eat local fish and game, because
their flesh now is contaminated at toxic levels with anthropogenic
carcinogens such as PCBs. In some places, one cannot drink the
water, for the same reason. In parts of Akwesasne, residents have
been told to plow under their gardens and to have mothers’ breast
milk tested for contamination. In place of sustaining rivers and a
land to which the Mohawks still offer thanksgiving prayers, late-
twentieth-century capitalism has offered incinerators and dumps
for medical and industrial waste. Akwesasne, which straddles New
York State’s border with Quebec and Ontario, has become the most
polluted native reserve in Canada and a number-one toxic site in
the U.S. EPA’s Superfund list of sites badly needing cleanup.
Within the living memory of many people at Akwesasne, the Land
Where the Partridge Drums, has inherited the toxicological conse-
quences of General Motors (GM) waste lagoons in which animals
have been found with levels of PCBs in their fat that qualifies them
as toxic waste under U.S. EPA guidelines. Akwesasne has become
112 The Dirty Dozen
riskier to human health than most urban areas, a place where any
grouse still living may be more concerned about its heartbeat than
about its drumbeat (Johansen 1993).
Soon after the St. Lawrence Seaway opened during the middle
1950s, GM, Reynolds Metals Company, and the Aluminum Com-
pany of America (Alcoa) built plants directly upstream of Akwes-
asne. According to the state attorney general’s office, GM never
obtained a permit to operate its dumpsites (Thomas 2001).
Paul Thompson of Akwesasne remembers his childhood in a more
innocent time: In a cove off the St. Lawrence River, walleye pike
leaped upstream to spawn every April. His family bought fresh catch
from fishermen on the river’s banks, as they “peer[ed] into their
crates and pick[ed] out the evening supper: a perch, bass, or maybe
a sturgeon head for soup” (Sengupta 2001). Nearby sits a mound in
which Thompson’s brothers and sisters once had foraged. “They
plucked scrap metal and sold it in town for extra cash. They burned
the wood at home” (Sengupta 2001). At the time, no one at Akwes-
asne realized that the nearby GM engine-parts factory, built during
the 1950s, was turning the fish to toxic waste and the children’s
play mound into a toxic dump.
Nearby, Turtle Cove, an inlet leading into the St. Lawrence River,
was a favorite swimming hole for children at Akwesasne. In the
spring, boys, like generations before them, learned to spear bull-
head pike making their way through the cove to spawn. The cove,
which is a few feet from the GM foundry, is a swimming hole no
longer. Instead, it is one of GM’s toxic-waste dumps.
Dana Leigh Thompson grew up with a forty-foot GM waste heap
as a neighbor. The toxic hill slopes into Containment Cove, a local
swimming hole until tests revealed PCB levels many times toxic lim-
its. “There were three big rocks out there,” Thompson said. “When
we taught kids how to swim, they could swim out to the middle and
stand. It was an achievement” (Seely 2001).
Thompson and other local residents began to suspect toxicity in
GM’s waste dumps during the middle 1970s, but GM continued to
dump PCBs in the area without a state permit until 1986. Cleanup
efforts began about 1988 but have stalled over differing approaches
to the problem.
The installation of the temporary cap, during 1983, initiated
Thompson’s former playground into the ranks of federal Superfund
sites, as one of the most toxic (in this case, PCB-contaminated)
patches of ground in North America. During 1988, according to res-

idents of Akwesasne, “A crew of men, covered head to toe in white
spaceman-like suits, covered it [the mound] with an impermeable
sheath” (Sengupta 2001). Meant to be temporary (in place until the
dump was cleaned up) the capped mound remained in place thir-
teen years later.
At first, “I didn’t even know what PCBs were,” said Jim Ransom,
an Akwesasne resident and director of the Haudenosaunee Envi-
ronmental Task Force, an environmental group that advocates on
behalf of all Iroquois. “There was a high level of concern, but I think
that there was also a lot of unknowns because people didn’t know
what this chemical was and what it could do to us.” By the mid-
1980s, preliminary testing showed that it was no longer safe to eat
fish and wildlife caught in some areas of the reservation. Sheree
Bonaparte, then a young mother with a farm near the GM landfill,
laughed when GM first distributed bottled water to residents
(Thomas 2001). At first, she said, “Everybody kind of thought it was
ridiculous,” she said. “The water comes from the earth and it
seemed silly to go get it from a bottle” (Thomas 2001).
The Mohawks, state agencies, and area universities soon began
studying PCB levels in breast milk and in infants. “Those studies
proved beyond any shadow of a doubt that at the beginning of the
study, the Mohawks had significantly higher levels of PCBs,” said
David Carpenter, a professor of environmental health and toxicol-
ogy at the State University of New York at Albany (Thomas 2001).
Carpenter said that the Akwesasne Mohawks have higher-than-
average rates of some diseases that are associated with PCB con-
tamination. One such disease, hypothyroidism, is “strikingly
elevated,” Carpenter said (Thomas 2001). PCBs disrupt production
of thyroid hormones, which leads to hypothyroidism, a disorder that
can cause mental dullness, obesity, and learning disabilities in
children.
For more than a decade, GM and the Akwesasne Mohawks have
debated how best to clean up the company’s waste lagoons. The
company has suggested sealing the dumps permanently in place,
meanwhile also building a wall to prevent existing PCBs from mi-
grating to other parts of Akwesasne. Federal officials have approved
this plan, but GM requires access to the reservation to build the
wall. The Mohawks have denied access because they believe GM is
seeking a relatively inexpensive way out of a problem that requires
removal, completely, of all soil tainted by PCBs dumped there.
114 The Dirty Dozen
In the meantime, the U.S. EPA commended GM for moving dili-

gently to clean up its waste sites. GM found itself inching toward
agreement with the Mohawks’ solution. The company, for example,
did remove 23,000 cubic yards of polluted sediment from the St.
Lawrence River during 1995. During 2000 GM excavated contami-
nated sludge from inactive lagoons. By the end of 2001, the com-
pany was planning to have removed soil from the banks of the
Racquette River.
“This is the only place we have, and we’re going to be here forever,”
explained Ken Jock, director of the St. Regis Mohawk tribe’s envi-
ronmental division. “Our teachers have told us, when we make a
decision we have to look at how it affects the next seven generations.
It’s a different sense of time” (Sengupta 2001). Before the area was
so widely contaminated, fishing, hunting, and trapping “were some-
thing our parents had pride in handing down to our children,” Jock
said. Because Akwesasne residents have been advised by state of-
ficials not to eat local fish or game, fishing and hunting skills are
being lost. “It’s pretty important to our identity as a people” (Thomas
2001).
Scientists have concluded that even low levels of PCB exposure
here could cause more serious illnesses than previously thought.
“That small relationship we expect to see correlated with reduced
I.Q., with poor performance in school, with some abnormality in
growth, particularly sexual maturation, and increased susceptibil-
ity to certain chronic diseases such as thyroid disease and dia-
betes,” said Carpenter. “This has adversely affected their health”
(Sengupta 2001).
Thompson’s family has been wracked by illnesses that once were
very rare at Akwesasne. Thompson himself has diabetes. Four of
his five siblings have thyroid disorders of a type often aggravated by
PCBs. Thompson’s sister Marilyn had her thyroid gland removed
when a tumor was discovered there. All six of her children have
asthma; two of them also have learning disabilities; another suffers
from a thyroid condition. A two-year-old granddaughter of Thomp-
son was born with a muscle disorder that has affected her motor
skills. Another family member has experienced fourteen miscar-
riages (Sengupta 2001).
Rowena General of Akwesasne said the contamination has led to
a “health crisis” for the more than 10,000 people who live on the
reservation. “Recent analysis of clinical and hospital records on the
reservation shows an epidemic of thyroid problems and also the

incidence of cancers, diabetes and respiratory diseases is higher
than average,” General said (Associated Press 2001).
The distribution of certain chronic diseases at Akwesasne was
determined using computerized medical records of the St. Regis Mo-
hawk Health Services Clinic. Prevalence proportions, annual inci-
dence rates, and five-year incidence rates were computed for the
period January 1, 1992, to January 1, 1997, for asthma, diabetes
mellitus type II, hypothyroidism, and osteoarthritis. The study in-
dicated that hypothyroidism and diabetes
showed higher age-specific prevalence than in the general U.S. population.

Osteoarthritis was extremely frequent among people 60 years of age and
older, and it may also be elevated in prevalence in relation to the U.S. gen-
eral population. The incidence and prevalence trends of diabetes type II and
osteoarthritis were stationary, but those for asthma and hypothyroidism
showed increases over the study period. Morbidity from asthma and ac-
quired hypothyroidism should be monitored in the future and investigated
through analytic epidemiologic methods for a possible association with life-
style and environmental factors. (Negoita et al. 2001, 84)
A study conducted at Cornell University indicated that smoke-

stack effluvia from the Massena Reynolds Metals factory also de-
stroyed once-profitable cattle and dairy farms in Cornwall on the
Ontario side of Akwesasne. The study linked fluorides to the demise
of cattle as early as 1978. Many of the cattle, as well as fish, suffered
from fluoride poisoning that weakened their bones and decayed
their teeth. Ernest Benedict’s Herefords died while giving birth,
while Noah Point’s cattle lost their teeth and Mohawk fishermen
landed perch and bass with deformed spines and large ulcers on
their skins. The fluoride was a by-product of a large aluminum
smelter in Massena, New York, that routinely fills the air with yel-
lowish gray fumes smelling of acid and metal (Krook and Maylin
1979).
Although Reynolds Metals, owner of the aluminum smelter, cut
its fluoride emissions from 300 pounds an hour in 1959 to 75
pounds an hour in 1980, the few cattle still feeding in the area con-
tinued to die of fluoride poisoning. The pollution of Akwesasne is
accentuated by the fact that most of the plants emitting toxins are
west of the reservation, upstream and often upwind.
Chronic fluoride poisoning in Cornwall Island cattle was “mani-
fested clinically by stunted growth and dental fluorosis to a degree
116 The Dirty Dozen
of severe interference with drinking and mastication. Cows died at

or were slaughtered after the third pregnancy. . . . Concentrations
exceeding 10,000 p.p.m. fluoride were recorded in cancellous bone
of a 4- to 5-year-old cow” (Krook and Maylin 1979, 1).
During late March 2001 New York Attorney General Eliot Spitzer
and the St. Regis Mohawk Nation gave notice to GM that he would
sue the company in federal court unless it began cleaning up two
PCB dumpsites at its Massena plant within ninety days. In a letter
to GM, Spitzer said if the company does not make substantial prog-
ress within ninety days, he would ask a U.S. District Court judge in
Albany to declare the site an “imminent and substantial endanger-
ment” and order an immediate cleanup (Associated Press 2001).
“General Motors has been on notice since at least 1980 that PCBs
were being released into the St. Lawrence River and onto the St.
Regis Mohawk Reservation from its two hazardous waste dumps,”
Spitzer said. “The company also has known for the past 15 years
that the landfills may endanger public health and the environment.
Despite this knowledge, GM has failed to control the release of these
toxins from its property” (Associated Press 2001).
By June, barely within its ninety-day deadline, the attorney gen-
eral’s office said that GM was taking PCB-removal talks with a new
sense of seriousness. “If we have to, we are ready to file a lawsuit at
a moment’s notice, and G.M. knows that we are prepared to do so,
if necessary,” said Marc Violette of the New York Attorney General’s
office (“State, G.M.” 2001).
Chris Amato, the assistant New York attorney general working on
the case, said the injustice is clear. “This is another example of a
Native American community being treated as second-class citi-
zens,” he said. “I guarantee you if this site was located next to a very
middle-class, white neighborhood, this site would be well on its way
to being remediated” (Thomas 2001).
“General Motors’ illegal industrial waste dump has been poison-
ing the Mohawk people for over 50 years,” said Akwesasne Mohawk
Loran Thompson. “Despite all of our efforts, the G.M. facility con-
tinues to discharge toxic contaminants into the Akwesasne envi-
ronment. General Motors is guilty of environmental injustice and
they have been completely negligent in overlooking the damages to
the health, well-being, economy, and lifestyle of the Mohawk people”
(Associated Press 2001).
OUR DAILY DIOXIN: LIFE AND DEATH IN

LOUISIANA’S “CANCER ALLEY”
The nickname Cancer Alley has been applied to a stretch of the
Mississippi River between Baton Rouge and New Orleans, Louisi-
ana, which includes several mostly low-income, mainly African-
American communities in the shadows of petrochemical and plastic
industries. Fourteen of fifteen U.S. plants that produce vinyl chlo-
ride monomer (VCM) and ethylene dichloride (EDC), the basic build-
ing blocks used to make polyvinyl chloride (PVC), are in Louisiana
and Texas. A large number of the incinerators that burn discarded
PVC products also are located in low-income minority communities.
Dioxin and dioxin-like pollutants, including PCBs, are unintention-
ally produced and released into the air and water and in hazardous
waste during the manufacture of VCM, the incineration of vinyl
products, and the burning of PVC in accidental fires.
The manufacture of polyvinyl chloride produces copious amounts
of dioxins, which “have been linked to immune-system suppression,
reproductive disorders, a variety of cancers, and endometriosis,”
according to one observer, who continued: “Dioxins are an unavoid-
able consequence of making PVC. Dioxins created by PVC produc-
tion are released by on-site incinerators, flares, boilers, wastewater
treatment systems and even in trace quantities in vinyl resins”
(Costner 1995). Products manufactured with PVCs “create dioxins
when burned, leach toxic additives during use . . . and are the least
recyclable of all major plastics” (Cray and Hardin 1998). “The pro-
duction of the carcinogenic monomer is what results in the highest
levels of dioxin release,” says Charlie Cray, a Greenpeace toxics
campaigner (Shintech 1999).
As early as November 1983, a U.S. EPA contractor (Versar 1983)
learned that the production of vinyl feed stocks (ethylene dichloride
and vinyl chloride monomer—EDC/VCM) was an inadvertent source
of PCB production. Hinting that the entire lifecycle of PVC should
be examined more intensely for PCB contamination, Versar also
concluded that “it would be necessary to consider input PCBs con-
taminating chlorinated feed stocks in further downstream process-
ing” (Dioxin Deception 2001). In 1990, however, at the request of
the Vinyl Institute and other VCM producers, the EPA deleted dioxin
from the list of constituents of concern in a VCM waste stream
because of “the costs of analysis and the reluctance of waste-
118 The Dirty Dozen
treatment facilities to take wastes designated as dioxin-

contaminated” (Dioxin Deception 2001).
During 1987, 106 residents of Reveilletown, Louisiana, a small
African-American community about ten miles south of Baton
Rouge, filed a lawsuit against Georgia Pacific and Georgia Gulf ar-
guing that they had suffered health problems and property damage.
After settling out of court for an undisclosed amount, Georgia Gulf
relocated the remaining families and then tore down every structure
in town. Management at Dow Chemical’s neighboring factory in Pla-
quemine followed suit soon afterward, buying out all the residents
of the small town of Morrisonville (Bowermaster 1993).
The PVC plants incinerate dioxin-contaminated wastes, and in so
doing, according to Greenpeace, a portion of the originally dis-
charged dioxins are emitted undestroyed, and new dioxins are cre-
ated as by-products of the incineration process. The presence of
copper and other metals in PVC industry wastes can act as a cata-
lyst to further increase dioxin formation (Duchin 1997). Under
usual operating conditions, several chemicals are burned in a con-
stantly changing mixture, creating a variety of synergistic chemical-
thermal reactions and emissions.
Greenpeace has called on the U.S. EPA to “impose a moratorium
on permits for new vinyl facilities or expansion of existing facilities,
and to modify permits at existing plants to require that dioxin re-
leases to all media, including waste destined for disposal, be
brought to zero within five years” (Duchin 1997). Greenpeace ad-
vocates a ban on the use of PVC in many types of toys, as well as
furniture, wallpaper, and medical devices such as intravenous
bags. Moreover, Greenpeace has called for a ban of PVC in products
that may be susceptible to fire, such as cabling and other construc-
tion materials, notably in appliances and vehicles; and “metals with
PVC residues that are recycled in combustion-based processes (i.e.,
automobiles)” (Duchin 1997).
During September 1998 Greenpeace activists joined the people of
Covenant, Louisiana, three-quarters of whom are black, in celebra-
tion of the news that the Japanese chemical giant Shintech would
not, after all, build an enormous, 3,000-acre polyvinyl chloride
(PVC) factory in their town. Shintech, a Japanese chemical com-
pany, had been trying since 1996 to locate three factories and an
incinerator near homes and schools in Covenant. Local people ar-
gued against location of the plant in their town on civil-rights
grounds; they argued that Louisiana authorities would violate

federal civil-rights laws if they licensed the Shintech plant in a
predominantly African-American community where pollution is
already making people sick (Cray and Harden 1998). This struggle
was undertaken with the idea of providing other poor minority com-
munities with legal precedents that would be useful in fending off
expansion of environmentally intrusive industries.
The proposed PVC plant would have been one of the largest of its
type in the world. Local residents worried most about anticipated
emissions of polyvinyl chloride (PVC), ethylene dichloride (EDC),
and vinyl chloride monomer (VCM) which “may reasonably be an-
ticipated to result in an increase in mortality or an increase in se-
rious irreversible, or incapacitating reversible illness. Vinyl chloride
is a known human carcinogen which causes a rare cancer of the
liver” (U.S. Environmental Protection Agency 1998). According to
the company, the proposed Shintech manufacturing plant would
have released about 600,000 pounds of toxic chemicals into the air
per year and would have poured nearly 8 million gallons of toxic
wastewater each day into the Mississippi River, which provides
drinking water for the city of New Orleans (Public Notice n.d.).
Greenpeace’s campaign against dioxins began during the 1980s.
In 1988 the Greenpeace ship MC Beluga toured Cancer Alley. In
1989, Greenpeace also released the report We all Live Downstream,
documenting serious chemical pollution in the Mississippi River
(Costner and Thornton 1989). During the middle and late 1990s,
Greenpeace activists, often swimming at night in polluted water,
sampled effluent from several U.S. vinyl producers and found di-
oxins at each of the twenty-seven sites tested.
One sample, obtained at the Vulcan Chemicals facility in Geismar,
Louisiana, contained 6 p.p.m. of TEQ dioxin, a level as high as the
historic levels in wastes left from Agent Orange production (Dioxin
Deception 2001). “These data are important, since they add to the
growing body of evidence pointing to the lifecycle of polyvinyl chlo-
ride (PVC) plastic as one of the largest single sources of the nation’s
total dioxin burden” (Duchin 1997).
Concentrations of dioxins in some of the samples taken by Green-
peace were extraordinarily high:
• Vulcan Chemicals, Geismar, Louisiana: 200,750 p.p.b. dioxins in a sam-

ple of “heavy end” waste
120 The Dirty Dozen
• Formosa Plastics, Point Comfort, Texas: 761 p.p.b. dioxins in a sample of

“heavy end” waste
• Georgia Gulf, Plaquemine, Louisiana: 1,248 p.p.b. dioxins in a waste sam-
ple from a tank labeled to contain “heavy ends,” “tars,” and other similar
types of highly contaminated wastes (Duchin 1997)
On occasion, Greenpeace also blockaded trains transporting vinyl

chloride at PPG Industries with two buses as it called for global elim-
ination of dioxin and other persistent poisons. Of twenty-eight res-
idents whose blood was tested by the federal agency, twelve had
elevated levels of dioxin or similar substances (“Louisiana Town”
n.d.). A Greenpeace Web page asserted that “Cancers, respiratory
problems, reproductive disorders are among those illnesses asso-
ciated with dioxin contamination, and which are occurring with
alarming frequency in Mossville” (“U.S. Government” 1999). By
1998 and 1999 Greenpeace was organizing toxic patrols with com-
munity activists to monitor chemical plants along the Mississippi
and on the shores of Lake Charles.
Residents in Covenant turned their backs on arguments that the
plant would provide them more jobs and economic prosperity. They
argued that the town already hosts a bevy of high-technology in-
dustries that emit various toxins, yet 40 percent of the townspeople
live below the poverty line. Most of the plants are highly automated
with little need for workers possessing marginal skills. Instead, the
plants tend to hire a few people (usually from the outside) with com-
puter skills and a working knowledge of physics and chemistry.
Shintech’s controller, Dick Mason, said the new complex would
bring with it 165 permanent jobs; the company also promised to
spend $500,000 for local job training, even though Louisiana offi-
cials had agreed to give Shintech $130 million in tax breaks without
setting any specific goals to commit the company to local hiring.
The state of Louisiana strongly supported Shintech’s plans; its
air, water, and coastal zone permits were granted, swiftly, “with the
backing of nearly all the relevant state and local officials, and over
the objections of over 18 groups and a large segment of the local
population” (Sierra Club n.d.). In a precedent-setting decision dur-
ing September 1997, the U.S. EPA rejected the state air permit. The
EPA found forty-nine deficiencies in the state’s granting of the per-
mit. The EPA also challenged state officials on questions of environ-
mental racism in siting the plant. Represented by the Tulane
Environmental Law Clinic, citizens’ groups filed appeals to the air,
water, and coastal-zone permits, “citing official bias as well as tech-

nical and legal problems” (Sierra Club n.d.).
Local citizens also lodged a complaint under Title VI of the U.S.
Civil Rights Act. The thirty-three-page complaint
[A]sserts that statements and actions by Governor Foster, DED Secretary

Kevin Reilly (the Governor’s liaison on the Shintech matter), Secretary Giv-
ens and other DEQ officials and employees create bias, prejudice or interest
toward Shintech and against the citizen groups and eliminate the legally-
required appearance of complete fairness and impartiality. The pervasive
evidence of bias or prejudice includes threats and investigations by the Gov-
ernor and Mr. Reilly against plant supporters and the Tulane Environmen-
tal Law Clinic, and an extensive, taxpayer-financed effort by the DEQ
Secretary’s office to organize and assist a group in St. James to support
Shintech and oppose the efforts of the community groups that object to the
proposed facility. (Sierra Club n.d.)
Covenant’s situation was grist for precedent; a review of 1990 cen-

sus data “shows that communities living near the nation’s existing
15 EDC/VCM facilities have a 55 percent higher percentage of peo-
ple of color than the national average, and a 24 percent lower per
capita income than the national average” (Sierra Club n.d.).
After the EPA rejected its air permit, the Louisiana Department of
Environmental Quality was required, by law, to convene public
hearings on Shintech’s application. Nearly three hundred citizens
attended the hearings in Covenant on December 9, 1996. Testimony
continued for more than eight hours, according to one account, “at
least 95 percent” against Shintech (Sierra Club n.d.). “Enough is
enough,” testified Patricia Melancon, president of the local group,
St. James Citizens, “This is a low-income area, and less than half
of the adults in this community have a high-school diploma. We will
get all of the pollution, but none of the jobs” (Cray 1996).
To demonstrate public support at the hearing, Shintech flew in
more than forty employees from its Freeport, Texas, plant as well as
its paid consultants, whose testimony centered on potential em-
ployment and tax revenue from the company’s proposal. “Why are
they [Shintech] speaking of economic development at an air permit
hearing?” asked Kishi Animashaun, Greenpeace Toxics campaigner
(Cray 1996).
After withdrawing from Covenant, Shintech switched its building
plans to Plaquemine, thirty miles north, where its executives hoped
that local opinion would be more accommodating. Shintech said it
122 The Dirty Dozen
planned to buy vinyl chloride monomer (feedstock finished PVC)

from a Dow Chemical plant in Plaquemine. People in Plaquemine
then organized People Reaching Out to Eliminate Shintech’s Toxins
(PROTEST). In their opposition to new PVC manufacturing there,
the members of PROTEST cited already-high cancer rates in the
town, falling property values, and a lack of emergency evacuation
routes should an accident occur. Liz Avants, speaking for PROTEST,
said, “Every day, we hear about more cases of cancer and other
health effects” (Shintech 1999).
A study released during 1999 by the Agency for Toxic Substances
and Disease Control (ATSDC) indicated that dioxin levels in Moss-
ville, one community in Cancer Alley (near Lake Charles), showed
that the average concentration of dioxins and PCBs in the blood of
its residents were three times the average level in the general
population.
On March 5, 1999, sixty Greenpeace activists from twenty-two
nations converged on the Louisiana State House to call attention to
global health and environmental threats caused by Louisiana’s nu-
merous polluting PVC production facilities. Dressed in T-shirts with
the slogan “Love Louisiana but Not PVC” in sixteen languages, the
Greenpeace Toxic Patrol called on Governor Mike Foster to clean up
the state’s Cancer Alley. The group then marched with local envi-
ronmental activists from the Capitol to the governor’s mansion to
deliver a “lunch” of contaminated fish and water from some of the
state’s most polluted waterways (“Louisiana’s Cancer” 1999).
Greenpeace on June 22, 1999, launched a Toxics Patrol bus trip
to more than a dozen of the state’s chemical facilities whose emis-
sions have made Louisiana a global toxic hot spot. The bus tour
began with stops at three controversial facilities: Rhodia, the na-
tion’s first napalm incinerator; Formosa, which makes components
of vinyl; and Dow Chemical, another vinyl producer that planned to
join with Shintech on a newly proposed vinyl plant in West Baton
Rouge. With representatives of several state and local environmen-
tal groups, Greenpeace displayed posted signs at chemical facilities
warning that toxic pollution “does not stop at the fence” (“With Pub-
lic’s” 1999).
“Louisiana ranks number one in the nation in per-capita toxic
releases to the environment, and her citizens are bearing a terrible
health burden for it,” said Greenpeace toxics campaigner Damu
Smith. “Our Toxics Patrol is out to expose some of the state’s worst
toxic offenders. . . . Louisiana is at the center of the nation’s growing

problem of environmental racism and injustice” (“With Public’s”
1999).
Acclaimed author Alice Walker, actress Alfre Woodard, actor Mike
Farrell, Rev. Al Sharpton, and members of Congress Maxine Waters
and John Conyers toured Cancer Alley on June 9, 2001 (“Celebri-
ties” n.d.). After the walking tour, the delegation convened in New
Orleans for the first-ever national town meeting on environmental
justice with residents, government officials, and representatives of
the chemical industry. During the town meeting, the delegation
heard personal testimonies of industrial contamination victims who
live in Cancer Alley communities that are experiencing illnesses and
social problems associated with toxic pollution. The town meeting
was coordinated and sponsored by Greenpeace (“Celebrities” 2001).
Bill Moyers’s report “Trade Secrets,” aired on the Public Broad-
casting System on March 26, 2001, described the lives and deaths
of some Cancer Alley workers, such as Ray Reynolds, forty-three
years old, who was shown in the living room of his house a few miles
from the chemical plant where he worked for sixteen years. Rey-
nolds was shown dying of toxic neuropathy that had spread from
his nerve cells to his brain. Another worker, Dan Ross, made his
living for twenty-three years producing the raw vinyl chloride that
is basic to the manufacture of PVC plastic. In 1989 Ross was told
he had a rare form of brain cancer.
Corporate documents displayed by Moyers indicated that manu-
facturers of PVCs knew as early as 1959 that “500 parts per million
is going to produce rather appreciable injury when inhaled seven
hours a day, five days a week for an extended period” (Moyers 2001).
As the years went by, the level at which exposure to PVC and other
organochlorines were believed to cause injury to the human body
crept downward. In 1959 workers were regularly exposed to at least
500 p.p.m. during their work shifts. Some workers described stand-
ing in clouds of the chemical at levels much above 500 p.p.m. Some
X-rays showed workers’ bones dissolving.
“Trade Secrets” included interviews with people affected by di-
oxins resulting from the manufacture of vinyl chloride, which draw
on an archive of secret and confidential documents unearthed in a
lawsuit by the widow of a Louisiana chemical worker. A 1959 memo
to the B. F. Goodrich Company, for example, says vinyl chloride “is
going to produce rather appreciable injury when inhaled seven
124 The Dirty Dozen
hours a day, five days a week for an extended period” (Kurtz 2001,
C-1).
U.S. TOXIC WASTES IN CANADA

Canada has been accepting shipments of PCB-contaminated
waste from American military bases in foreign countries that the
United States itself will not accept. Greenpeace International re-
leased a U.S. Defense Department document prepared for the U.S.
Congress during March 1999 that refers to “current shipments of
foreign-manufactured waste to Canada” (Rusnell 2000). “Green-
peace will be asking for a detailed summary of all the American mili-
tary waste that has been coming into Canada and for how long,”
said Darryl Luscombe, a toxic-waste campaigner in Ottawa who ob-
tained the document. “This also raises the question of where this
waste has been going in Canada” (Rusnell 2000).
A U.S. company, Trans-Cycle Industries, was known to have
shipped eighty-one tons of PCB-contaminated waste from a U.S.
military base in Japan to Canada. The shipment, aboard a Chinese
bulk carrier, arrived at the port of Vancouver, British Columbia, on
April 8, 1999. The waste was then trucked to the company’s plant
at Kirkland Lake in northern Ontario. Trans-Cycle had no approval
from Ontario to import hazardous waste from outside Canada. In
fact, Ontario’s Environment Department had denied the company’s
foreign-waste import application.
In 1997 the United States closed its borders to PCBs. Under Ca-
nadian environmental law, waste containing fewer than 50 parts per
million of PCBs can be imported from any of the 130 countries that
signed the Basel Convention, an international agreement meant to
control the movement of hazardous waste around the world.
More than 200 truckloads of U.S. toxic waste undergoing treat-
ment in Alberta became a target of controversy there as environ-
mentalists and a city alderman wondered whether an accident
might occur as the waste was en route to Swan Hills, 500 kilometers
northwest of Calgary. “It could cause a tremendous health hazard
if you had a truckload of [persistent organic chemicals] or PCBs go
down,” said Margaret Chandler, editor of the Alberta environmental
magazine Encompass (Rusnell 2000).
Bovar Inc.’s Swan Hills Treatment Center is finalizing contracts
and permits. Swan Hills was being prepared to receive POPs such
as DDT and other pesticides from the Pacific Northwest. Bovar has
been given government approval to treat PCBs and other toxic
chemicals from outside Canada. During 2000, Bovar burned 3,000
to 5,000 tons—up to 250 truckloads—of foreign toxic waste at its
facility, according to its president, John Kuziak. “We cannot afford
to have an incident on the roads. That would really cause people to
be concerned, so we take very careful precautions,” Kuziak said
(Pierson 2000, 4).
“GIFT WASTE” AND THIRD WORLD

COUNTRIES
Tanzania has become home to huge stockpiles of agricultural pes-
ticides and veterinary drugs, including such compounds as DDT,
which pose a threat to the environment and to the public’s health.
Some stocks are more than thirty years old and are stored with few
or no safety precautions. Stocks of toxic chemicals have been grow-
ing in Tanzania because there is no environmentally sound way to
dispose of them. “Environmental and health experts warn that un-
less quick action is taken, the situation could be catastrophic,”
according to a Los Angeles Times report (Simmons 2000). Envi-
ronmentalists estimate that Tanzania has more than five hundred
tons of agricultural compounds dumped or stored at more than a
hundred sites (Simmons 2000). Most of the material was imported
more than a decade ago as donations by China, Japan, Italy, the
United States, and other wealthier countries seeking to dispose of
chemicals that now are illegal, and unusable, at home.
The scope of the gift waste problem has been growing. During
early May 2001 the United Nations Food and Agriculture Organi-
zation (FAO) said that more than 500,000 tons of banned or expired
pesticides are seriously threatening the environment and the health
of millions of people worldwide in developing countries. This was
five times FAO’s previous estimate. “In Asia,” according to an FAO
news release, “The quantities of obsolete pesticides are estimated at
over 200,000 tons, in Africa and the Near East at over 100,000 tons,
and in Eastern Europe and the former Soviet Union at more than
200,000 tons” (FAO 2001).
“The lethal legacy of obsolete pesticides is alarming and urgent
action is needed to clean up waste dumps,” said Alemayehu Wod-
ageneh, an FAO expert on obsolete pesticides. “These ‘forgotten’
126 The Dirty Dozen
stocks are not only a hazard to people’s health but they also con-
taminate natural resources like water and soil. Leaking pesticides
can poison a very large area, making it unfit for crop production”
(FAO 2001). In its new report, FAO calls upon chemical companies
represented by the Global Crop Protection Federation (GCPF), to aid
global disposal of pesticides produced by GCPF member companies.
“Support from industry is crucial for the future disposal of pesti-
cides because aid agencies of donor countries cannot cover all the
costs without a substantial contribution from industry,” the FAO
expert said (FAO 2001).
During the mid-1970s to 1980s, pesticides were sold to many Af-
rican nations to improve agricultural production. At the time, the
pesticides were offered “hand in hand with friendly donors wanting
to help,” when the effects of the toxins were not widely known (Sim-
mons 2000). Today, “much is stockpiled in tattered sacks or in leak-
ing and corroding metal drums near settlements. Some of the stores
are located near rivers, irrigation schemes or ports; others are
stashed outdoors in mountainous piles. Worn or missing labels
make it impossible to determine the exact content of some contain-
ers” (Simmons 2000). During the last thirty years, pesticides have
seeped into soil, groundwater, and irrigation projects, entering the
food chain near many storage areas.
“One nightmare scenario would be some cataclysmic meteorolog-
ical event that would wash [or] disperse large quantities of DDT or
another persistent pesticide into the environment, where the effects
could last for many, many years,” said Richard Liroff, Washington-
based director of the World Wildlife Fund’s Alternatives to DDT Proj-
ect (Simmons 2000).
PCB RUSTLING IN ZAMBIA

The Environment News Service reported on September 1, 2000,
that the Zambia Electricity Supply Corporation (ZESCO), the sole
supplier of hydroelectric power in Zambia, had warned the public
against unscrupulous people stealing oil containing PCBs from the
company’s transformers. According to Mellon Chinjila, an official at
ZESCO Environment and Social Affairs Unit in Lusaka, the contam-
inated oil was being sold on the open market in Zambia as cooking
oil and skin-lightening lotion. At Nkana Copper Mines, traces of oil
thought to contain PCBs were noted around the walls of a building
where the theft of thousands of liters of PCB-contaminated oil was

reported. Chinjila warned that although this oil may look like gen-
uine cooking oil, it can cause human organ damage and infertility
in both men and women. “ZESCO has in the past months been dis-
tributing awareness materials on the potential dangers of PCBs to
human health and the environment,” Chinjila said (Hanyona 2000).
ORGANOCHLORINES IN SOUTH ASIA

Life-threatening poisons such as DDT, aldrin, chlordane, diel-
drin, and heptachlor—all of which are either severely restricted or
banned in most countries—continue to be manufactured, stored,
used, and traded freely in South Asia, according to an investigative
report released by Greenpeace, titled Toxic Legacies, Poisoned Fu-
tures: Persistent Organic Pollutants in Asia (Hernandez and Jayar-
aman 1998).
“Asia faces a frightening scenario of historic, current and poten-
tial poisoning by the most dangerous variety of persistent poisons.
This situation is a result of existing stockpiles of obsolete pesticides,
the continuing production of organochlorines and other chemical
pesticides and the unmitigated expansion of dirty chlorine-based
industries in the region,” said Nityanand Jayaraman, a Greenpeace
campaigner (“Persistent” 1998).
Greenpeace investigations conducted between April and August
1998 in seven Asian countries, including Bangladesh, India, Nepal,
and Pakistan, revealed that stocks of at least five thousand metric
tons of obsolete pesticides had been stored under extremely haz-
ardous conditions in more than a thousand sites in Pakistan and
Nepal. A sizeable portion of these pesticides arrived as part of aid
packages from western countries, and almost all the pesticides were
exported by developed nations and India to Pakistan and Nepal.
Chemical corporations whose products were identified in stock-
piles in Pakistan and Nepal by Greenpeace investigators included
Bayer and Hoechst (Germany); DuPont, Dow Chemical, Diamond
Shamrock, and Velsicol (USA); Shell (Netherlands); Sumitomo
Chemical and Takeda Chemical (Japan); Rhône-Poulenc (France);
Sandoz (Switzerland); ICI (United Kingdom); and Bharat Pulverising
Mills (India).
India is among the three remaining manufacturers of DDT in the
world, the other two being Mexico and China. India during the late
128 The Dirty Dozen
1990s exported nearly 800,000 kilograms of organochlorine pesti-

cides including aldrin, DDT, BHC, and chlordane to a long list of
countries, including countries where their usage is banned. Exports
of pesticides that could be branded POPs in the near future such as
endosulfan, sodium pentachlorophenate, 2,4-D, and lindane total
more than 2 million tons. Some of the pesticides such as aldrin are
not permitted even to be manufactured in India. In Pakistan, India,
Nepal, and Bangladesh, locally banned or severely restricted pes-
ticides are freely available. Greenpeace found DDT, BHC, dieldrin,
and heptachlor openly sold in vegetable markets in Karachi. Hard-
ware stores in New Delhi stock the deadly pesticide aldrin, whose
registration was withdrawn there more than two years ago.
“It is unfortunate that while governments in the region are still
grappling for ways to dispose of their stockpiles of obsolete imported
pesticides, the continuing production and trade of these chemicals
goes on unabated. This could only lead to an endless cycle of poi-
soning whose unwitting and eventual victims are communities and
future generations,” said Jack Weinberg, international toxics cam-
paigner with Greenpeace. “Governments should aim for an eventual
phase-out of such polluting practices and push for international
cooperation in developing viable and sustainable non-chemical al-
ternatives” (“Persistent” 1998).
CONCLUSION: COMING TOGETHER

Friends and neighbors in minority communities across the United
States often have found themselves making common cause to evict
organochlorine chemicals from their communities. In so doing, they
often have found themselves coming together, becoming organized,
sharing strategy and tactics, and speaking out against several forms
of racism. In this process, leaders have arisen.
One such leader is Mildred Bahati McClain, executive director of
the People of Color and Disenfranchised, who describes herself as
a “mother, grandmother and a steward of my community,” (Mc-
Clain, n.d.). McClain, who lives in Savannah, Georgia, also is a
singer who has enthralled many audiences.
McClain said of her childhood:
I grew up in Savannah smelling the stench from the Union Camp Paper
Company thinking the smell was a natural part of life. My mother’s friends
who lived near Union Camp were always complaining of headaches, bad
skin rashes, kidney problems and severe cases of asthma. . . . I am frus-

trated because we are clearly being discriminated against. Many think we
are crying wolf, but I ask you to come to our neighborhoods and see for
yourself. You will be in shock. (McClain, n.d.)
McClain has become a major organizer of resistance to
organochlorine-manufacturing plants in minority communities, no-
tably in the southern regions of the United States. Along the way,
she and her supporters have made some political points about ra-
cism as well. McClain tells the following story about a meeting in
New Orleans:
On Sunday morning . . . several Cherokee Indians were treated miserably
in a Shoneys restaurant. They were ignored and then received only partial
and reluctant service. When this was made known to those attending the
conference, participants quickly organized a march involving over 200 peo-
ple. We went to the restaurant to demand an apology. In a very moving
meeting, the tearful manageress apologized and said it would never happen
again. It felt really good on that march. We had Native Americans, African
Americans, Asian Americans, Hispanic Americans and White Americans
marching together. It felt like a microcosm of what we had to do. Just after
we got back to the hotel, the heavens opened. Native Americans saw this as
a “cleansing.” (Work on Waste 1996)
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5
Belugas with Tumors: The Toxic
Toll on Animals
We live in a world that now offers no refuge from the synthetic chem-
ical effluent of industry—a fact that is attested, again and again, by
levels of various POPs in the body fat of mammals, such as polar
bears, which live thousands of miles from the factories producing
the chemicals and most of the people who use them. Meat-eating
birds, such as bald eagles and vultures, also are unwilling world-
wide witnesses to the spread of DDT, PCBs, dioxins, and other syn-
thetics into the entirety of the biosphere.
Such is the ecological state of a world in which vultures (in India)
die from eating DDT-contaminated cattle carrion. In today’s world,
PCB toxicity levels in whale meat are causing some of its major con-
sumers, the Japanese, to become leery of eating it. Toxicity, more
than any human “green” consciousness, thus may be “saving” the
whales, at least for the time being. Whales, like all mammals, pass
their toxic burden to offspring, in concentrated form, imperiling
each successive generation with greater potential for cancers, re-
productive failure, and other maladies that follow from increased
POP toxicity. We live in an ecological world in which beluga whales
grow cancerous tumors, a world in which, sometimes, not even an
informed observer can tell which polar bears are male and which
are female.
An extensive body of scientific evidence has documented the dev-
astating toll of persistent organic contaminants on wildlife. In many
parts of the world, wild species show signs of disrupted sexual de-
velopment and a diminished ability to reproduce. Some sensitive
species have disappeared altogether because of total reproductive
failure linked to some of the dirty dozen chemicals on the POPs list.
134 The Dirty Dozen
One well-informed observer believes that “Evidence is conclusive

that dioxin (TCDD) causes cancer in animals” (Allsopp, Costner, and
Johnston 1995).
In laboratory animals, exposure to dioxins, particularly 2,3,7,8-
TCDD (a form of dioxin), has been associated with a large number
of toxic effects. Some of these effects have occurred at very low
doses. For instance, exposure of monkeys to only 5 parts per trillion
of 2,3,7,8-TCDD caused impaired neurological development and
endometriosis (Rier et al. 1993). Pregnant rats receiving a single
small dose of 2,3,7,8-TCDD on day fifteen of pregnancy had male
offspring that appeared normal at birth but at puberty were “de-
masculinized, with altered reproductive anatomy, reduced sperm
count, feminized hormonal responses, and feminized sexual behav-
ior” (Mably et al. 1991; Thornton 1997). In 1992, researchers at the
University of Wisconsin reported that low-level prenatal exposures
to dioxin feminized the behavior of male rats during adulthood and
sharply reduced their production of sperm (Mably et al. 1992a).
Very low doses of dioxin also have produced immune-system
changes in rats and monkeys (Hong, Taylor, and Abanour 1989;
Neubert et al. 1992; Yang, Lebrec, and Burleson 1994). Reproduc-
tive function may be disrupted by exposure to PCBs in animals,
especially mammals (including humans). Female rhesus monkeys
exposed to PCBs “have alterations in menstrual cycles (e.g., dura-
tion and bleeding), decreases in fertility, increased abortions and
reductions in the number of conceptions” (Arnold, Mes, and Bryce
1990; Barsotti, Marlar, and Allen 1976).
PCBs have been implicated in the disappearance or decline of sev-
eral animal species in the United States and Europe. Mink, for ex-
ample, began disappearing from the shoreline of the Great Lakes
during the mid-1950s. Despite restrictions on DDT, PCBs, and
other POPs, mink have not yet returned. At the same time, British
researchers have linked PCBs to the decline of otters in Britain and
Europe during the 1950s (Lopez-Martin, Ruiz-Olmo, and Minano
1994). Mink are very sensitive to reproductive impairment induced
by prenatal organochlorine chemical exposure.
Dioxins and PCBs are toxic to the immune systems of many ani-
mals. Many studies support evidence that exposure to extremely
low doses of dioxin increases susceptibility to bacterial, viral, par-
asitic, and neoplastic diseases (U.S. EPA, 1994). Many of these
Belugas with Tumors 135
chemicals also act as endocrine disrupters, some of whose effects

are alligators born with abnormally small penises and birds with
crossed beaks. Endocrine disrupters confuse the body’s sexual
identity. Effects of endocrine disruption include interrupted sexual
development, thyroid-system disorders, inability to breed, reduced
immune-system response, and abnormal mating and parenting be-
havior. Some species for which abnormalities have been reported
include terns, gulls, harbor seals, bald eagles, beluga whales, lake
trout, panthers, alligators, turtles, and others.
Bald eagles around the Great Lakes and in the Columbia River
basin in Washington State were unable to reproduce successfully
after they were fed local fish for two or more years. The bodies of the
fish-eating bald eagles have been contaminated with enough DDT,
PCBs, and chlordane to compromise their reproductive capacities,
despite the fact that all these chemicals had been banned for twenty
years by the time measurements were taken during the early 1990s
(Montague 1993). The chemicals continued to be imported into the
United States from countries still manufacturing them, and existing
stocks are very persistent. “PCBs will be around over geologic
time”—thousands of years—one report asserts (Colborn et al. 1993,
378).
In all mammals, male and female reproductive organs are par-
ticularly at risk during fetal development after maternal exposure
to organochlorines. The reproductive organs at risk are the mam-
mary glands, uterus, cervix, and vagina in women and the seminal
vesicles, prostate, epididymides, and testes in men. The skeleton,
thyroid, liver, kidney, and immune systems are affected in both
sexes.
A fetus grows rapidly and is therefore very susceptible to damage
from toxic insults. Damage to the dividing cells of a developing fetus
often causes severe deformity. Not only is the fetus growing rapidly,
but it also has little body fat, no protective reservoir for fat-soluble
toxins such as organochlorines, as in adults. Enzyme systems are
immature, so a fetus can detoxify toxic substances at a rate too low
to compensate for exposure. Permanent effects are most likely to
arise from exposure during this point in the life cycle. These effects
may be immediately apparent, such as deformities at birth. Many
effects also may not become obvious until the offspring exposed pre-
natally reaches maturity (Colborn et al. 1993).
136 The Dirty Dozen
PITY THE POLAR BEAR

Pity the polar bear, whose food supply (mainly seals) now arrive
less often on receding ice, and whose body fat has become contam-
inated, more so generation by generation, with chemical toxins such
as dioxins and PCBs that bioaccumulate along its food chain. The
polar bears are subject to the same environmental stresses as the
Inuit with less ingenuity to outwit the pending environmental apoc-
alypse in the Arctic. We may be able to count the polar bear gener-
ations to extinction on one set of human fingers if production and
use of persistent organic pollutants is not stopped soon.
As with Inuit mothers, polar bears’ offspring are one step of bio-
magnification along the food chain:
Stiff and lean after six months curled in a den, a female polar bear squeezes
herself out of her winter home. Two small cubs emerge tentatively at her
heel for their first view of the world beyond a snow cave. Entirely dependent
on their mother, the cubs follow obediently. Having used up most of her fat
stores, the female scans the sea ice below and ponders a meal of seal blub-
ber. But her cubs are not yet ready to travel, and her milk will have to
sustain them for some time to come. The milk is rich and nourishing but
today it also harbors a threat. The seals that the mother has feasted on in
the past, and will need to eat again soon, are tainted by chemicals from
lands far beyond her sea-ice domain. The chemicals that bind to the fat of
the seals have accumulated in her own fat stores. Unwittingly, the mother
passes the toxins to her young in her fat-rich milk, with effects that are still
unclear. (“Persistent Organic” n.d.)
Polar bears sit at the top of a major food chain in the Arctic, an
area that has become a major sink, or repository, for POP contam-
ination generated at lower latitudes. If an animal’s milk-fat content
is higher, the magnification of POPs such as dioxin and PCBs is
higher; POP concentrations in dolphins accelerate more quickly
through the generations than for human beings, because their milk
is richer in fat-harboring contaminants. Polar bears and seals, as
well as other Arctic or Antarctic mammals, feed their offspring a fat-
contaminated toxic cocktail of POPs.
Increasing POP levels among some polar bears already have, in
some cases, transformed their sexual organs, confusing male and
female. Scientists on the Svalbard islands have found that more
than one in a hundred of the islands’ polar bears are hermaphro-
ditic. The condition, in which an animal possesses the reproductive
organs of both sexes, afflicts wildlife in various parts of the world.
It may be caused by exposure to chemicals that affect the endocrine

system.
PCBs probably are responsible for the Svalbard bears’ physiolog-
ical sexual confusion. The same pollutants also are compromising
the bears’ immune systems. This phenomenon was unknown a de-
cade ago on the islands, which lie between Norway and the North
Pole. By the year 2000, 1.2 percent of Svalbard’s bears, which total
about 3,000, had two sets of sexual organs (Kirby 2000). Per Kyrre
Reymert, of the Svalbard Science Forum, told BBC News Online:
“Tests have been conducted on 40 bears, and these are now being
analyzed. There is a very short and simple food chain here—plank-
ton, fish, seals, and finally the bears themselves. So it is fairly easy
to track PCBs and other pollutants” (Kirby 2000).
Elizabeth Salter, of the World Wildlife Fund, told British Broad-
casting Corporation News Online: “It seems to be the female bears
on Svalbard that are acquiring male genitalia, a penis-like stump.
. . . what’s happening to the bears is happening to gulls in the Arctic,
too, because of PCBs, DDT and dioxins” (Kirby 2000). Per Kyrre Rey-
mert fears there will be more encounters between humans and
bears. “Climate change is likely to reduce the amount of ice around
Svalbard. With less ice, there will be more bears coming ashore. And
they will be hungry,” Reymert said (Kirby 2000).
Polar bears are among several predatory marine mammals that
consume high levels of organochlorines. Organochlorine chemicals
including DDT, PCBs, chlordanes, HCHOs, and PCCOs (polychlo-
rinated camphenes, e.g., toxaphene) have been widespread in the
Arctic, affecting fur seals (Callorhinus ursinus), ringed seals (Phoca
hispida), hooded seals (Cystophora cristata), bearded seals (Erig-
nathus barbatus), walrus (Odobenus rosmarus divergens), beluga
(Delphinapterus leucas), porpoises (Phocoena phocoena), narwhal
(Monodon monoceros), and polar bears (Ursus maritimus). All are
relatively high on their respective food chains and very susceptible
to bioaccumulation of these organochlorines. In the Wadden Sea,
reproductive failure of the common seal (Phoca vitulina) and sub-
sequent population decline has been attributed to PCBs (Norstrom
and Muir 1994).
HEAVY METALS IN ALASKAN REINDEER

The Seward Peninsula of Alaska has been extensively mined for
the last hundred years. The mining of cadmium- and lead-bearing
138 The Dirty Dozen
ores and the widespread use of these two elements for industrial
purposes have significantly increased environmental contamina-
tion over the last century. These elements are readily absorbed by
plants that are in turn eaten by ungulates, concentrating in liver,
kidney, and muscle tissue. In some cases, health officials have rec-
ommended against consumption of reindeer meat, after learning
that contamination from weapons testing, accidental pollution, and
illegal dumping may have found their way to the lichens of North-
western Alaska. The same contamination also has accumulated in
reindeer and caribou tissue (“Heavy Metal” 2000).
Many people on Alaska’s Seward Peninsula live a subsistence life-
style with most of their food coming from local plants and animals.
The incidence of cancer and other diseases appears to be rising
among the native people in this region. “Though the link between
epidemiology and environmental factors potentially involves a mul-
titude of causal relationships, the people in the villages are particu-
larly concerned that contaminants from air pollution, mining
operations, and dumpsites are concentrating in the tissue of sub-
sistence animals and pose a health risk” (“Heavy Metal” 2000). The
Reindeer Research Program detected high levels of cadmium and
lead in several species. At similar concentrations, consumption of
forty to sixty grams of meat per week would exceed the recom-
mended intake rate (“Heavy Metal” 2000). Similarly, reindeer and
pike in northern Sweden were found to be contaminated with ra-
dioactivity after the nuclear accident at Chernobyl in the Ukraine
(Forberg, Tjelvar, and Olsson 1991; Skogland 1987).
BELUGAS WITH TUMORS

While levels of various industrial chemicals (notably PCBs) in the
St. Lawrence River have declined since the 1960s, Beluga whales
still show high levels of toxicity, with higher concentrations in
younger whales. These findings indicate that these contaminants
are being transferred across the placenta from mother to offspring.
The belugas’ fatty breast milk has been bioaccumulating toxins
across generations long after human injection of POPs into the river
decreased substantially. In this way, young belugas acquire a toxic
load much higher than their parents’ in the absence of new PCB
contamination. Researchers found one beluga in the St. Lawrence
that had 500 p.p.m. of PCBs in its body fat, ten times the concen-
tration required to classify it as toxic waste under Canadian envi-

ronmental law (Colborn, Dumanoski, and Myers 1996).
In the St. Lawrence River, beluga whales suffer from an astonish-
ing list of afflictions—several kinds of cancer, twisted spines and
skeletal disorders, ulcers, pneumonia, bacterial and viral infec-
tions, thyroid abnormalities—seldom if ever seen in belugas living
in less-polluted water. Ongoing research on this population indi-
cates that widespread hormone disruption is undermining repro-
duction and preventing recovery of the population (World Wildlife
Fund 2000).
During the past decade, scientists also have found that contam-
inants such as DDT, PCBs, and dioxins weaken the immune sys-
tems of marine mammals. This evidence now makes it appear likely
that contaminant-induced immune suppression may have contrib-
uted to the dramatic marine epidemics that killed thousands of
seals, dolphins, and porpoises in the late 1980s and early 1990s.
The dramatic die-offs hit populations in the Baltic and North Seas,
the Mediterranean, the Gulf of Mexico, the North Atlantic, and the
eastern coast of Australia. The carnage extended even to seals in
Siberia’s Lake Baikal.
MALE FISH SECRETING FEMALE HORMONES

During the 1980s, John Sumpter, a professor of biochemistry at
Britain’s Brunel University, found male fish secreting female hor-
mones in the River Lea, which runs through an industrialized sec-
tion of North London. The bodies of the male fish were creating large
amounts of the female egg-yolk protein vitellogenin. Usually males
do not make any of this substance. “The levels of vitellogenin in the
blood of the males was extraordinarily high, increased by about
100,000 times. The levels reached are those we would normally ex-
pect to find in a fully mature female trout which was making lots of
eggs,” said Sumpter (Cadbury 1997, 114). Sumpter and his col-
leagues analyzed sewage and other discharges into the River Lea
and were among the first to link synthetic estrogens to the femini-
zation of male fish. Female mollusks (e.g., snails and mussels) have
become male after exposure to endocrine-disrupting chemicals (a
condition known as imposex).
When caged trout were placed downstream from sewage treat-
ment plants in several British rivers, the males developed excessive
140 The Dirty Dozen
levels of vitellogenin in their blood (Purdom et al. 1994; Sumpter

1995). Every sewage-treatment plant in England caused this estro-
genic effect within two to three weeks’ exposure. The British re-
searchers found that several common industrial chemicals produce
vitellogenin in male fish under laboratory conditions: octylphenol
and nonylphenol (both alkyl phenols, used in detergents, toiletries,
lubricants, and spermicides); bisphenol-A (used in polycarbonate
plastics); DDT (the common pesticide); and Arachlor 1221, one of
the 209 varieties of PCBs (Sumpter and Jobling 1995). The same
researchers also tested chemical mixtures and found that the
mixtures were more powerful progenitors of vitellogenin than any
of the individual chemicals alone. These studies also documented
bioaccumulation of the chemicals. Thus, a weakly estrogenic chem-
ical could eventually build to a level capable of producing vitel-
logenin.
Sumpter and Jobling also tested for estrogenic effects in fish
across species. They concluded that “Most evidence supports the
idea that if a chemical is estrogenic in one species, it will be in all
others” (Montague 1997a). Late in 1996, researchers in the United
States published studies confirming that sewage-treatment effluent
there also can cause the same effects in fish living downstream (Fol-
mar et al. 1996).
Scientists examined male carp from five locations in the Missis-
sippi River downstream from a Minneapolis sewage-treatment
plant, as well as from a tributary, the Minnesota River, which bears
intense agricultural chemical runoff. They found that carp living
near the Minneapolis sewage-treatment plant showed “a pro-
nounced estrogenic effect,” producing vitellogenin along with re-
duced levels of testosterone (Folmar et al. 1996, 1096). In addition,
the site with the highest level of dissolved pesticides in the United
States (as tested by the U.S. Geological Survey), the Platte River at
Louisville, Nebraska, had the lowest estrogen-to-testosterone ratio
in the United States (Montague 1997a).
Infusion of dioxins and furans into the marine environment from
neighboring industrial plants caused a particularly high level of
contamination among crabs in a Norwegian fjord. Similar levels of
contamination have been noted in Newark Bay, New York Bight, and
Tokyo Bay. For freshwater fish, studies on various rivers showed
that in Spain, heptachlor epoxide exceeded World Health Organi-
zation (WHO) standards; in Australia, PCBs and chlordane also ex-
ceeded WHO standards. Fish taken from the St. Lawrence River and
rivers in British Colombia had higher than usual concentrations of
dioxins and furans for their areas and the world as a whole. In
southern Taiwan, fish taken from a river and culture ponds ex-
ceeded dioxin standards as a result of industrial activities in the
area.
POPS AND THE DECLINE OF FROG

POPULATIONS
Pesticide residues drifting up Sierra Nevada slopes from Califor-
nia’s agricultural valleys have been linked to drastically declining
frog populations there. Researchers from the U.S. Geological Survey
and the U.S. Department of Agriculture assert that the pesticides
disrupt an enzyme that regulates the frogs’ nervous systems. Frog
populations have been reported to be in decline (with an upsurge in
deformities, such as extra or missing limbs) in many areas, but this
study is among the first to assay a cause for a specific amphibian
decline. Commented biologist Jessa Netting, writing in Nature, “Am-
phibians, with their moist, sensitive skins, unprotected eggs, and
semi-aquatic lifestyle, have long been viewed as biological indicators
of environmental health” (Netting 2000, 760). Ultraviolet radiation
and parasites also are suspected factors in other frog-population
declines.
Industrial toxins, notably agricultural herbicides, are one of sev-
eral factors contributing to widespread frog population declines and
deformities worldwide. Froglog, published by the Species Survival
Commission of the Declining Amphibian Populations Task Force of
the World Conservation Union has reported that the 1996 Red List
of Threatened Animals (published by the International Union for
Conservation of Nature) listed 156 amphibian species as extinct,
critical, endangered, or vulnerable to extinction. This represents 25
percent of all the amphibians on Earth (Halliday 1997). The Nature
Conservancy, a U.S. organization, in 1996 surveyed the status of
20,481 species of plants and animals in the United States and re-
ported that 37.9 percent of U.S. amphibians are in danger of becom-
ing extinct (Dicke 1996).
Researchers at Widener University in Chester, Pennsylvania, and
at Benedictine College in Atchison, Kansas, have shown that acid
rain can stress frog populations by harming their immune systems
142 The Dirty Dozen
(Brodkin and Simon 1997). According to one observer, frogs raised

in water with a pH of 5.5 had significantly more bacteria in their
spleens and a significantly higher death rate than frogs raised in
waters with a pH of 7.0. The researchers attribute the increased
numbers of bacteria to reduced efficiency of bacteria removal by
white blood cells—part of the frogs’ immune defenses (Chow 1997;
Montague 1998).
High levels of organochlorine pesticides have been correlated with
reduced frog populations in several parks and wildlife reserves
along the northern edge of Lake Erie. At Point Pelee National Park
in Canada, only five frog species remain; DDT residues in these frogs
average 5,000 to 47,000 micrograms of DDT per kilogram of body
weight (Russell and Hecnar 1996; Russell et al. 1995, 1997).
During the early 1990s, researchers discovered many frogs and
toads with missing back legs in ponds and ditches exposed to pes-
ticide runoff in the St. Lawrence River valley in Quebec, Canada.
Twelve percent of the frogs examined in one study had hind-limb
deformations that are otherwise “virtually unknown” among am-
phibians in the wild (Ouellet et al. 1997, 95). In 1997 the Australian
government banned eighty-four herbicide products for use near wa-
ter because of their harmful effects on tadpoles and frogs (Tyler
1997). Researchers in Sri Lanka have reported that frogs are nearly
absent on tea plantations where herbicides are used intensively. Sri
Lanka frog populations rebounded quickly after spraying stopped.
“Conversion to pesticide-free tea production in this region has con-
tributed greatly to the re-establishment of populations of local
frogs,” according to this study (Senanayake et al. 1997, 2).
Peter Montague has observed that “All of the banned products
contain Monsanto’s glyphosate as the active ingredient. However,
the harmful component appears to be not the glyphosate itself but
an ‘inert’ ingredient, a detergent or wetting agent added to the her-
bicides so that droplets of liquid spread out and cover the target
leaves. Detergents interfere with the ability of frogs to breathe
through their skins, and tadpoles to breathe through their gills”
(Montague 1998). Michael J. Tyler of the Department of Zoology at
the University of Adelaide, Australia, says, “Although the herbicide
[glyphosate] is claimed to be ‘environmentally friendly,’ it is clear
that users have been lulled into a false sense of security” (Montague
1998).
ATRAZINE, FROGS, AND SEXUAL

DYSFUNCTION
Atrazine (2-chloro-4-ethytlamino-6-isopropylamine-1,3,5-triazine),
the most frequently used herbicide in the United States, has been
associated with a wide array of sexual abnormalities in frogs by a
study published in the Proceedings of the U.S. National Academy of
Sciences. Tyrone B. Hayes, a specialist in the hormone systems of
amphibians at the University of California at Berkeley, led the team
who conducted the study. Laboratory experiments there suggest
that even at very low levels, exposure to atrazine can disrupt hor-
mones and alter the sexual development of male African clawed
frogs.
The study was published as the U.S. Environmental Protection
Agency entered the final phase of its special review of the chemical,
begun during 1994 after atrazine was found to be widespread in
U.S. drinking water. Although atrazine has not been proven as dan-
gerous to humans as to frogs, studies compiled by the U.S. Geolog-
ical Survey have detected levels as much as 2,300 p.p.b. in drinking
water consumed near some agricultural areas. The EPA has at-
tempted to limit drinking-water concentrations to 3 p.p.b.
The Hayes team’s findings indicate that atrazine is a powerful
endocrine disrupter in frogs. Exposure of tadpoles to water with
0.1 p.p.b. of atrazine, or 30 times less than the amount legally per-
mitted in drinking water, induced male frogs to develop both testes
and ovaries. “The atrazine turns on an enzyme called aromatase,”
Hayes said. “This converts testosterone to estrogen” (Green 2002,
A-16). Roughly 20 percent of the frogs that the Hayes team tested
showed hermaphroditic characteristics, a number the team has dis-
covered translates into 40 percent of the population’s males.
“We have males with up to six testes, for example,” Hayes said.
“We have animals with three testes and three ovaries” (Nelson 2002,
A-20). When exposed to 1 part atrazine per billion parts water,
Hayes said 90 percent of the male frogs suffered a deficient voice
box. Because frogs sing to attract mates, the deficiency poses a ma-
jor handicap. “No song, no offspring,” Hayes said (Nelson 2002, A-
20). At 25 p.p.b. of atrazine, a level frequently observed in rainfall
and surface waters in some midwestern agricultural areas, Hayes
and colleagues found that sexually mature males suffered a tenfold
decrease in testosterone, a decline that Hayes said amounts to
“functionally castrating the animals” (Nelson 2002, A-20).
144 The Dirty Dozen
Sensitivity of frogs to atrazine at levels of a few p.p.b. is important

because intense agricultural use of the chemical has caused it to
become part of the natural background. Atrazine was, by the year
2000, being used in eighty countries around the world. Atrazine has
generally been regarded as relatively safe because of its short half-
life and low rate of biomagnification. In human adults, a sketchy
test record has indicated that it causes abnormalities only at very
high doses (Hayes et al. 2002, 5476).
Hayes and his colleagues found atrazine present at a saturation
of “several parts per million in agricultural runoff, and [as much as]
40 parts per billion in precipitation” (Hayes et al. 2002, 5476). By
contrast, according to tests by Hayes and colleagues, “by immersion
throughout larval development,” deformations of male frogs’ sexual
organs (hermaphroditism and demasculinization) began at any level
more than 1 p.p.b., a level that is now present in precipitation even
in areas where it is not used (Hayes et al. 2002, 5476). According to
Hayes et al., at a level of 25 p.p.b., male Xenopus laevis (African
clawed frogs) suffered a 10-fold decrease in testosterone levels.
Syngenta, the company that manufactures most of the atrazine
sold in the United States, funded some of Hayes’s early research
under pressure from the EPA but rejected its results. Syngenta tox-
icologist Tim Panoor said other studies commissioned by the firm
produced contrary results. “No conclusions can be drawn,” he said
(Green 2002, A-16). Atrazine was first synthesized in Switzerland in
1955 and was licensed in the United States during 1959. Of the 75
million pounds now used in the United States every year, most are
applied in the Midwest on corn, sorghum, and sugarcane crops
(Green 2002, A-16). Atrazine has been banned in Switzerland, Swe-
den, Germany, Italy, Norway, France, and Belgium (Dalton 2001,
665).
“This is not a worst-case scenario where animals are exposed to
mega-doses,” commented Louis Guillette, a zoologist at the Univer-
sity of Florida in Gainesville, who has studied the effects of persis-
tent organic pollutants in alligators. “These are concentrations we
know wild amphibians are exposed to” (Dalton 2002, 665).
Scientists debating whether high rates of deformities in frogs are
the result of parasites or pollution may both be right, according to
a study published July 9, 2002, in the Proceedings of the National
Academy of Sciences. Penn State University biologist Joseph Kie-
secker wrote that infection with trematode worms, a common par-
asite, actually causes the deformities in wood frogs but that the
deformity rates were substantially higher in areas where infected
frogs were exposed to pesticide runoff” (“Links Found” 2002). Kie-
secker said the chemicals may lower frogs’ immunity to infection,
or pesticide runoff may boost the population snails that transmit
the trematodes to frogs.
Kiesecker’s study examined frogs in six central Pennsylvania
ponds. Some had pesticide runoff, and some did not. Results from
the wild were compared to frogs in the lab. In ponds without pesti-
cide runoff, deformities occurred in 5 percent to 10 percent of
trematode-infected frogs. In ponds where runoff was present, de-
formity rates ranged from 20 percent to 30 percent (“Links Found”
2002). In the wild, deformities occurred only where the parasite
could get at the frogs—confirming the parasite’s essential role in the
malformations, Kiesecker reported in the Proceedings of the Na-
tional Academy of Sciences.
“If it’s true that commonly used pesticides compromise the im-
mune system of a vertebrate organism, which is what these findings
suggest, then we’re looking at a much bigger problem than de-
formed frogs,” said David Gardiner of the University of California at
Irvine (Souder 2002, A-9). The pesticide concentrations used in this
study fell below government-recommended levels for safe drinking
water. Among them was atrazine, the most heavily used agricultural
herbicide in the United States.
According to a report in the Washington Post, “In the lab, Kie-
secker found much higher rates of parasitic infection in tadpoles
exposed to pesticides, along with a matching reduction in white
blood cell production—an indication of a weakened immune re-
sponse. Frogs exposed to pesticides were also smaller and developed
more slowly. Kiesecker said inhibited growth rates might also con-
tribute to deformities seen in the field by creating a longer ‘window’
when parasitic infection could affect limb development” (Souder
2002, A-9).
“The original purpose of these experiments was to study how dis-
ease in aquatic systems impacts growth and development,” Kie-
secker said. “To be honest, we were quite surprised to see limb
deformities and this strong pattern of interaction between parasites
and pesticides” (Souder 2002, A-9). “Amphibians have become an
important model system,” Kiesecker said. “We have to consider that
factors that influence infection rates in frogs may also play a role in
human diseases” (Souder 2002, A-9).
146 The Dirty Dozen
Kiesecker’s results contradicted tests sponsored by Syngenta

Crop Protection Inc., a manufacturer of atrazine, which failed to
support a conclusion that the chemical is causing widespread de-
formation of frogs. The studies were unable to replicate the results
of earlier research that alleged that atrazine may affect the larynx
and sexual development of African clawed frogs. The studies were
conducted by a panel of eight university scientists convened by
Ecorisk—a global network of environmental scientists—to examine
the environmental effects of atrazine (“UV Radiation” 2002).
“As research on this issue continues, one thing is certain,” said
Ronald Kendall, director of the Institute of Environmental and Hu-
man Health at Texas Tech University and chair of the science panel.
“No conclusions can be drawn at this time on atrazine and its pur-
ported effect on frogs. We must get the science done in order to have
the facts to make sound conclusions” (“UV Radiation” 2002).
DIOXINS AND ENDOMETRIOSIS

Permanent exposure to low levels of dioxin can cause endometri-
osis in monkeys (Montague 1993). Endometriosis is a painful dis-
ease of the tissues lining the uterus, which often results in sterility;
it presently afflicts 5 to 9 million women in the United States. Male
rats exposed to PCBs prior to birth have disturbed thyroid hor-
mones; as a side effect, these rats have small testicles and reduced
sperm counts as adults (Montague 1993). Exposure of rodents to
endocrine-disrupting chemicals “can cause them to undergo pu-
berty at an early age and can cause persistent estrus [being ‘in heat’]
for a . . . prolonged time,” according to the Weybridge Report, a key
compilation of pesticide effects on health (Montague 1997b).
Male rodents exposed to chemicals that interfere with androgens
(male sex hormones) can be born with hypospadias (a birth defect
of the penis) and cryptorchidism (undescended testicles) (Montague
1997b, part 1, p. 29). The Weybridge Report attributes these effects
to Vinclozolin, a powerful antiandrogenic pesticide. Remarks Peter
Montague: “In the United States today, Vinclozolin is legal for use
on cucumbers, grapes, lettuce, onions, bell peppers, raspberries,
strawberries, tomatoes, and Belgian endive. The U.S. Environmen-
tal Protection Agency has no published plans for banning Vinclo-
zolin” (Montague 1997b).
Furthermore, according to Peter Montague, “There is evidence
from a number of animal species that sex steroids (for example,
estrogen and testosterone) exert long-term effects on the size of the

thymus and on the immune system in general” (Montague 1993).
In humans, the thymus is an organ, just above the heart, that pro-
duces T cells, which are crucial actors in the immune system” (Mon-
tague 1997b).
CONTAMINATION IN NORTHERN FUR SEALS

The breeding rookeries for more than 70 percent of the world’s
population of northern fur seals (Callorhinus ursinus), in the Bering
Sea on the two largest Pribilof Islands (St. Paul and St. George,
Alaska) offer evidence of reproductive problems caused by organo-
chlorines. The St. Paul breeding population appears to have stabi-
lized after a decline of about 7 percent per year between 1975 and
1983. However, on St. George, pup production declined at an an-
nual rate of about 6 percent from 1973 to the middle 1990s (Beck-
men, Krahn, and Stott 1997). The Aleut village culture on these
islands is tightly bound to a subsistence harvest of the northern
fur seal.
Pregnant northern fur seals accumulate organochlorines during
winter feeding before their June migration to the Pribilofs to give
birth. While pregnant, females transfer organochlorine compounds
to their fetuses as they continue to accumulate new organochlorines
in their blubber. “During lactation,” wrote Beckmen and colleagues,
“not only is she mobilizing her highly OC [organochlorine]-
contaminated blubber, she is also transferring to her pup OCs ac-
quired from foraging around the Pribilofs” (Beckmen, Krahn, and
Stott 1997). Bioaccumulated organochlorines also have been found
in many of the seals’ food sources, including squid, pollack, herring,
and salmon. Squid had the highest levels of dioxins among this
group and salmon the lowest.
Pregnant fur seals accumulate the contaminants, passing them
to their offspring in mother’s milk, and thus, according to Kimberlee
Beckmen and colleagues (1997), “Northern fur seal pups receive the
highest doses of OC exposure in utero and in the neonatal period.
Studies in humans and laboratory animals indicate this is a period
when the immune and neurological systems are in critical devel-
opmental stages and are extremely sensitive to permanent damage
from low-dose exposures of environmental contaminants.”
Beckmen and colleagues (1997) wrote that “The northern fur seal
(Callorhinus ursinus) population that breeds on St. George Island,
148 The Dirty Dozen
Alaska, has been declining at an annual rate of approximately 6

percent per year since 1973. Previous studies have failed to identify
an exact cause, but have found lower-than-expected return rates
after initial post-weaning migrations. Since preliminary studies
suggested the need to examine the possibility of environmental
contaminant-linked immunosuppression, pups and their dams
were sampled during the 1996 breeding season on St. George Is-
land” (Beckmen, Krahn, and Stott 1997).
POPS AND ANIMALS OF THE GREAT LAKES

The Great lakes of North America have become a nerve center for
study of toxic hot spots affecting animals that have been exposed to
POPs. Dioxins, for example, now appear to have been responsible
to some degree for the extinction of the native lake trout in the Great
Lakes. Fishery officials earlier had blamed the trout’s population
crash during the 1950s on overfishing, habitat destruction, and
predation by an introduced parasite, the sea lamprey.
Research in the Great Lakes Basin on persistent toxic substances
has shown population decreases in wildlife, increased mortality
rates, reproductive problems, genital malformations, birth defects
such as cross-billed ducks, and tumors in fish. Impacts on human
health include the presence of toxic substances in breast milk, in-
creased incidence of cancer, and changes to the human reproduc-
tive system.
Theodora Colborn earned a doctorate in zoology from the Univer-
sity of Wisconsin during her fifties (in the 1980s) and got a job sur-
veying the environmental health of the Great Lakes. Much of the
visible pollution of the Great Lakes system had been dealt with by
that time; the days were over when a river in Cleveland could catch
fire (as it did in 1969) and create sensational headlines. By the late
1980s, many people thought the Great Lakes were being brought
back to environmental health.
After two months immersing herself in reports of animal health in
the Great Lakes, Colborn was convinced that the proclamations
were premature.
She had come to doubt that the lakes, however improved, were truly
“cleaned up.” The broken eggs littering the bird colonies may have disap-
peared, but biologists working in the field were still reporting things that
were far from normal: vanished mink populations; unhatched eggs, defor-
mities such as crossed bills, missing eyes, and clubbed feet in cormorants,
and a puzzling indifference in usually vigilant nesting birds about their in-
cubating eggs. (Colborn, Dumanoski, and Myers 1996, 14)
Colborn was beginning to trace many reports that would later as-
sociate a wave of seal deaths in northern Europe with a large num-
ber of deaths among striped dolphins in the Mediterranean Sea. She
would find the common ties between these extinctions and exami-
nations of deformed sperm in Denmark.
At roughly the same time Colborn was suspecting that something
was amiss in the Great Lakes, Niels Skakkebaek, a reproductive
researcher at the University of Copenhagen, was searching for rea-
sons why the rate of testicular cancer had risen threefold in Den-
mark between the 1940s and the 1980s. He was peering through
microscopes at sperm samples that “might have two heads [and]
. . . two tails, while another might have no head at all” (Colborn,
Dumanoski, and Myers 1996, 9). Along the way, he would discover
that worldwide human sperm counts seemed to be declining signifi-
cantly, as much as 50 percent in half a century.
Between 1950 and 1980, the seal population collapsed near the
mouth of the Rhine River. Per Reinjders, a Dutch biologist, found
impaired reproductive capacity in seals living in the western
reaches of the Wadden Sea, into which the Rhine River was pouring
PCBs and other organochlorines. Most often, fertilized eggs failed to
implant in the seal mothers’ uteri.
In gull and tern colonies in the Great Lakes, the Pacific Northwest,
California, and Massachusetts, field researchers have found nests
with twice the usual number of eggs, which is a sign that the birds
occupying the nests were two females instead of the expected male-
female pair. In some Lake Ontario colonies, birds showed behavioral
aberrations, including less inclination to defend their nests or sit
on their eggs, which increased predation and diminished the hatch-
ing and survival of chicks.
POPS AND ALLIGATORS IN FLORIDA’S

LAKE APOPKA
POPs have been linked to stunted penises and reproductive fail-
ure in the alligators of Florida’s Lake Apopka. Alligator eggs col-
lected there had relatively high levels of a variety of contaminants,
150 The Dirty Dozen
including toxaphene, dieldrin, and the DDT breakdown products

DDE and DDD. Abnormally small penises were the most dramatic
symptom of a profound but otherwise invisible disruption of the al-
ligators’ internal reproductive organs resulting from skewed hor-
mone levels. These problems were later found among alligators in
other Florida lakes as well, but nowhere else as intensely as at Lake
Apopka, which experienced a chemical spill in its recent history.
Discovery of alligator hormone abnormalities and reproductive fail-
ure in other Florida lakes indicates that chronic contamination from
agricultural pesticides may be as hazardous (and on a much wider
scale) than individual chemical spills.
Lake Apopka, contaminated by pesticide and herbicide runoff as
well as an extensive spill of the organochlorines dicofol and DDT,
suffered a progressive decline of its alligator population that began
during the 1980s and continued into the 1990s. By 1995 the alli-
gator population of the lake had declined 90 percent from its 1970s
levels. Estrogen levels in young female alligators in Lake Apopka
were found to be twice those of alligators in an unpolluted lake. Lake
Apopka alligators also have experienced abnormal ovarian struc-
tures. Male juveniles had significantly depressed levels of testoster-
one (three times lower than controls), poorly organized testes, and
small penises. Gonads of juvenile male alligators have been per-
manently altered during fetal development, disrupting production
of sex hormones that govern sexual differentiation (Guillette et al.
1994).
Louis Guillette of the University of Florida, who studies alligator
deformities, said that healthy alligators might have eggs that were
75 percent healthy and 25 percent dead or deformed. When scien-
tists began to study the alligators in Lake Apopka, they found that
nearly 90 percent of their eggs had died (Cadbury 1997, 124).
Many Lake Apopka alligators also were found to be “intersex,”
having mixed gender characteristics. An intersex male might have
a penis and testes but also produce female hormones. In some
cases, testes resembled ovaries. According to Guillette, “Almost 80
percent of the male alligators caught on this lake have some kind of
abnormal phallus or abnormal penis” (Cadbury 1997, 126). Some
of the animals changed their sex during embryonic development.
The same problems seemed also to afflict other animals in Lake
Apopka. Turtles, for example, were about 25 percent intersex, ac-
cording to Guillette (Cadbury 1997, 126).
Alligator reproductive problems have come to light all across

southern Florida (CNN 1998). In the Everglades, which are contam-
inated with numerous pesticides, “full-grown alligators weigh
hundreds of pounds less than alligators elsewhere in Florida”
(Montague 1998). In this area, juvenile alligators have levels of re-
productive hormones in their blood that are far below normal. Male
alligators exposed to pesticides in Florida are having difficulty re-
producing, partly because their penises are not developing to nor-
mal size. Males of many wildlife species of birds, fish, amphibians,
and mammals are said to have been feminized by exposure to low
levels of pesticides and other industrial chemicals (Raloff 1992,
1993, 1994).
Panthers in Florida’s Everglades National Park and Big Cypress
swamp have suffered from sterility and sperm abnormalities, mal-
functioning thyroid glands, and impaired immune response. Prob-
lems with undescended genitals in male cubs have increased
markedly since 1975, a result, perhaps, of the same pollution that
has been afflicting alligators in some of the same areas.
The Florida panther (Felis concolor coryi), an endangered species,
has been failing to reproduce. By the early 1990s, only thirty to fifty
Florida panthers remained. Researchers have reported that be-
tween 1985 and 1990, 67 percent of male panthers were born with
one or more undescended testicles, a condition known as cryptor-
chidism. In England and the United States, cryptorchidism has
more than doubled in men during the last four decades. Further-
more, some Florida panthers are sterile while others produced ab-
normal or deformed sperm (Giwercman and Skakkebaek 1992;
Montague 1994). These reports surfaced at nearly the same time as
reports asserting a 50 percent decline in human semen quality
(Carlsen et al. 1992).
A majority of the remaining Florida panthers have exhibited sev-
eral developmental abnormalities as well as reproductive defects.
Twelve males had low ejaculate volumes and low sperm concentra-
tions. A very high proportion (92.9 percent) of their sperm exhibited
morphological abnormalities. Female Florida panthers had high
body burdens of various contaminants, including DDE, PCBs, me-
thoxychlor, oxychlordane, and t-nonachlor. Reproductive abnor-
malities in the panthers may be due to contamination of the
mothers by endocrine-disrupting chemicals, according to one study
(Danish Ministry of Environment and Energy 1995).
152 The Dirty Dozen
DEATHS OF VULTURES IN INDIA AND DDT-

CONTAMINATED CARRION
In some areas of India, vultures have vanished because DDT con-
taminated their food chain (as well as that of human beings in the
area). Forty years after environmentalist Rachel Carson exposed the
dangers of DDT in Silent Spring, large amounts of the pesticide con-
tinue to be manufactured by India’s public-sector companies for
health programs. The chemical is still the only practical defense
against malaria in much of the tropical world. The Stockholm Con-
vention on POPs grants DDT an extended phase-out period because
of its vital role in containing malaria.
Investigations were begun during 1999 to determine why vultures
had vanished from the Keoladeo National Park in western Rajasthan
state, where they had been plentiful just a few years earlier. Vul-
tures, which feed on the carcasses of DDT-contaminated dead cows,
have been disappearing. DDT affects embryonic development in
birds directly or by reducing eggshell thickness as well as altering
mating and parenting behavior. “What is important to note is that
vultures and human beings share the same food chain and must
therefore be accumulating the same toxins,” said Anil Agarwal, an
investigator on the scene. “India’s apathetic administration is yet to
wake up to the pesticide threat” (Raj 2000).
India banned DDT for agricultural uses in 1998, but because it is
cheap, available, and easy to use, large quantities were still being
sprayed on crops two years later, according to Jagdish Prasad
Singh, pesticides expert at the Voluntary Health Association of India
(Raj 2000). Besides India, China and Mexico were still manufactur-
ing DDT in 2000. In the meantime, some pests have developed re-
sistance to DDT, as DDT levels rise in human populations where
the chemical is still being used, including India. Dr. T. S. Kathpal,
a pesticide chemist at the Haryana Agriculture University at Hissar,
believes that virtually no item of food available in India is now free
of DDT. Kathpal, who spent two decades tracking DDT contami-
nation in animals and human beings, said Indians now show a 22.8
p.p.m. body burden of DDT compared to 4.3 for Japanese 3.70 for
Australians and 2.24 for people in the United States (Raj 2000).
Greenpeace scientist Pat Costner asserted that DDT and other
POP chemicals pose a particular danger to infants in South Asian
countries because they interfere with lactation in mothers. “In
South Asian countries, breast-feeding is not a choice but the only
nutrition available to millions of newborns and the effect of POPs

on lactation can be disastrous,” Costner said (Raj 2000).
TOXICITY SAVED THE WHALES?

Toxic contamination may be saving some whales from extinction
because human consumers are avoiding them. The major consum-
ers of whale meat, the Japanese, began to question its safety after
high levels of heavy metals and chemicals were found in whale meat.
Some Japanese scientists advised against eating whale meat, and
sales declined. Japanese retailers, including one three-hundred-
store supermarket chain, were reported to be removing whale meat
from their shelves after scientists recommended an “immediate ban
on the sale of all contaminated products” (Lean 2000). The scientists
pointed out that toxic chemicals can bioaccumulate in whales and
dolphins to 70,000 times the levels found in the waters in which
they swim and feed.
Conservationists have been campaigning to stop whaling for
more than thirty years as unregulated whaling has forced many
species, such as bluefin and humpback, to the verge of extinction.
Consumer-driven hunting of these and other species has contin-
ued. During 1999, however, two Japanese toxicologists and two ge-
neticists from Harvard University analyzed more than one hundred
samples of the meat served or sold in restaurants, shops, and mar-
kets across Japan in a study coordinated by the British-based
Whale and Dolphin Conservation Society and the Swiss Coalition
for the Protection of Whales. According to a news account in the
London Independent, “They were astonished at the results. About
half of all the samples proved to be contaminated with heavy metals
or dangerous chemicals including mercury, dioxins, DDT and PCBs
above maximum levels allowed for human consumption under Jap-
anese and international standards” (Lean 2000).
During the mid- to late 1990s, a seven-year study in the Faeroe
Islands found that children whose mothers had eaten contaminated
whale meat during pregnancy were much more likely to suffer brain
and heart damage. During 2000 researchers led by Koichi Hara-
guchi, associate professor at Daiichi University’s College of Phar-
maceutical Sciences in Fukuoka, Japan, detected dioxin levels up
to 172 times the tolerable daily intake in whale and dolphin meat
that was offered for sale. Haraguchi’s team examined levels of dioxin
154 The Dirty Dozen
as well as dibenzofuran and coplanar polychlorinated biphenyl,

which have a degree of toxicity similar to that of dioxin, in thirty-
eight types of whale and dolphin meat sold in Japan during 1999
and 2000. The highest concentrations of dioxins were detected in
the fat of dolphins, at a maximum of 691 picograms per gram when
the amount was converted into the most toxic dioxin, and 232 pi-
cograms on average, according to the report (“Whale and Dolphin
Meat” 2000).
The World Wildlife Fund has warned that an initial toxic analysis
of Norwegian Minke whale meat and blubber samples destined for
human consumption revealed more than fifty polychlorinated bi-
phenyl (PCB) isomers, including some dioxin-like PCBs, which are
suspected endocrine disrupters (Allsopp, Costner, and Johnston
1995). The same tests also revealed twenty-five metals, including
organic mercury. The Convention for International Trade of Endan-
gered Species in Flora and Fauna (CITES) has rejected Norway’s
proposal to reopen international trade in whale products. Norway
has been holding blubber stockpiles in the hope that one day the
international ban on whale meat products may be lifted.
ESTROGENIC CHAOS: REPORTS ON SEVERAL

SPECIES
Exposure of pregnant rats to relatively low levels of dioxin did not
cause maternal toxicity but did permanently reduce their male off-
spring’s sperm counts. Testicular weight also was reduced. In an-
other study, these effects were shown to occur after a single very
low dose of dioxin (64 nanograms/kilogram) given on the fifteenth
day of pregnancy. No effect on other organ systems has ever been
observed at such a low dose. Mably and colleagues (1992a, 1992b)
concluded that the male reproductive system “is highly sensitive to
perinatal (prenatal and lactational) exposure of dioxins” (Allsopp,
Costner, and Johnston 1995).
Exposure to dioxins during pregnancy causes fetal death in mon-
keys and other small laboratory mammals. Prenatal exposure to
PCBs has been found to cause fetal malformations (teratogenic) in
laboratory mammals (Shane 1989). Exposure to the organochlorine
perchloroethylene (tetrachloroethylene), which is used in the dry-
cleaning industry, causes fetal death in rats and growth distur-
bances in mice (Schwetz, Leontg, and Gehring 1975). Breeding
difficulties in several species of sea fish have also been associated

with exposure to organochlorines, including PCBs, DDT, and DDE
(Johnston and McCrea 1992).
Chronic, long-term, low-dose exposure to dioxin in marmoset
monkeys resulted in changes in lymphocytes at body burdens of
only 6 to 8 nanogram per kilogram (Neubert et al. 1992). “Results
from such animal experiments are of concern because effects on the
immune system are occurring at body burdens similar to, or within
an order of magnitude of current human body burden estimates
(5–10 ng/kg), (U.S. EPA 1994). Female monkeys given a few mil-
lionths of a gram of dioxin showed a high incidence of abortions.
The same monkeys also developed bone-marrow abnormalities and
hemorrhages of the heart and lungs, as well as gangrene in their
toes and fingers. A report on this research observed that “After 33
months the monkeys were taken off the tests but continued to de-
teriorate. They lost their hair, their eyelids swelled up and, finally,
most of them died” (Cook and Kaufman 1982, 5).
POPS AND BALD EAGLES

The bald eagle has lived in North America for roughly a million
years as an opportunistic carnivore that usually eats carrion and
steals food gathered by other birds. The bald eagle also sometimes
eats small live birds and other animals. A bald eagle’s preferred diet
is rich in protein contaminated with fat—a perfect biological me-
dium for bioaccumulating POPs.
During the bald eagle’s million-year residency in North America,
the last century has been the most threatening to its survival as
a species. During the late nineteenth century, bounties were paid
for dead eagles, and their customary habitat was reduced by hu-
man encroachment. By the early twentieth century, the bird had
achieved a protected status as a U.S. national symbol and was re-
covering. During the 1940s, however, populations began to plunge
again with the onset of organochlorine pollution. The travails of the
eagle with DDT were chronicled in detail by Rachel Carson in Silent
Spring (1962). By the middle 1980s, fewer than fifty bald-eagle nest-
ing sites were known in the entire Great Lakes watershed (Colborn
et al. 1990).
Bald eagles around Lake Superior get an extra dollop of organo-
chlorine pollution because their diet is made up largely of fish-
156 The Dirty Dozen
eating gulls: “Because of this taste for gulls, they accumulate

concentrations of contaminants that are 20 times greater than they
would have if they had eaten only fish” (Colborn, Dumanoski, and
Myers 1996, 154). This level of toxicity is reflected in rising number
of deformed chicks even after (as in the case of St. Lawrence River
beluga whales) human-induced pollution had ceased or been re-
duced significantly.
Rachel Carson (1962) described how organochloric chemicals
cause eggshell thinning, increased embryo mortality and deformi-
ties, and caused feminization of males in many bird species.
Carson’s case centered on bald eagles, whose populations dropped
drastically during the 1950s and 1960s. The poisoning of avian spe-
cies that Carson described so graphically has continued and inten-
sified in some areas (note India’s dying vultures, above). Studies of
fish-eating bird species around the Great Lakes have shown that
eggs contain organochlorine pesticides, PCBs, and dioxins (PCDDs
and PCDFs) in concentrations high enough to cause adverse effects
on parents and their chicks. Bird populations in this area have been
declining since the 1950s (Giesy, Ludwig, and Tillitt 1994).
Gulls in Puget Sound and the Great Lakes have shown signs of
eggshell thinning and abnormalities of their reproductive tracts, in-
cluding feminization of male embryos. Populations have declined in
some areas, and sex ratios have been skewed. These areas are con-
taminated with residues of DDT, PCBs, and polycyclic aromatic hy-
drocarbons that may be responsible for these effects singly or in
combination (Fry 1995; Schettler et al. 1999, 156–58).
Despite restrictions on the use of DDT in the United States after
1972, embryonic and chick survival along the shore of the Great
Lakes continued, at least until about 1990, to be inadequate to
maintain stable populations among several bird species (Colborn,
vom Saal, and Soto 1993). Newly hatched male chicks from Lake
Ontario had testes resembling ovaries. In addition, female pairs of
gulls were found tending abnormally large clutches of eggs, most of
which were infertile.
Michael Fry of University of California at Davis has been observing
“lesbian gulls,” female-female pairs on Santa Barbara Island off the
California coast. Male gulls seem, according to Fry’s observations,
to have lost interest in mating and sex. Many male gulls display
feminized sex organs after they have been chemically castrated by
DDT and other environmental pollutants (Montague 1994).
ESTROGEN MIMICS AND ZEBRA FINCHES

Estrogen mimics have been implicated with masculinizing female
zebra finches and causing infertility in males of the same species.
The research indicates that zebra finches’ consumption of estrogen-
mimicking chemicals can alter the brains of the female birds enough
to make them sing. In nature, male finches sing to attract mates.
Scientists who fed female zebra finch hatchlings for a week with
estradiol, an estrogen hormone used in hormone replacement ther-
apy, produced singing birds (“Environmental Estrogens” 2002). Mil-
lions of women take estrogen supplements in birth-control pills and
in estrogen supplements to relieve hot flashes and other symptoms
of menopause. These pharmaceutical estrogens have been detected
in some cities’ treated sewage wastewater.
Dissecting the birds’ brains, the scientists discovered that the re-
gions controlling singing were well-developed in the females treated
with estradiol. The control group, given canola oil instead, showed
no such effect. Estradiol-treated male chicks were found to be in-
fertile as adults (“Environmental Estrogens” 2002). “These results
indicate that songbird populations may be at risk if they are exposed
to estrogenic chemicals as chicks,” said James Millam, professor in
the animal science department in the University of California at Da-
vis College of Agricultural and Environmental Sciences and lead au-
thor of the studies published in the December 2001 and April 2002
issues of the journal Hormones and Behavior (“Environmental Es-
trogens” 2002).
In an earlier study, Millam and colleagues found that estradiol
hindered the finches’ ability to reproduce. According to a report by
the Environment News Service, “Exposure to estradiol resulted in
fewer and more brittle eggs for the tested group and more infertile
eggs in groups containing estrogen treated males. As a result, the
number of hatchlings decreased compared to those of the control
group” (“Environmental Estrogens” 2002).
HOW CHEMICAL PESTICIDES SOMETIMES

INCREASE INSECT INFESTATIONS: THE
ARMYWORM
Malathion has been used to eradicate the boll weevil in the cotton
fields of the South, but in so doing it also nearly eradicated a wasp
that eats armyworms. As a result, a plague of armyworms in recent
158 The Dirty Dozen
years has driven some cotton farmers into bankruptcy. “It’s unbe-
lievable,” said Auburn University ornithologist Geoffrey E. Hill. “I’ve
literally seen them strip a field. There’s nothing left” (Williams 1999,
26). Philip Barbout, a Mississippi farmer, said that “In 1995 there
were so many, they were crawling up telephone poles” (Williams
1999, 26).
American Cyanamid has been requesting EPA approval to use Pi-
rate, a new chemical, one of a family called pyrroles. Pirate was be-
ing used in about thirty other countries (including Australia, China,
South Africa, Zambia, and Zimbabwe) by the year 2000. Some en-
vironmentalists have warned that chlorfenapyr, the active ingredi-
ent in Pirate, may be the next DDT. Like other organochlorines,
chlorfenapyr accumulates in animals’ body fat and disrupts their
endocrine and immune systems. The American Bird Conservancy
issued an action alert, requesting popular pressure on the EPA to
deny permission to sell and use Pirate. An EPA risk assessment has
said that residues of the chemical “present a substantial risk to
avian species for both acute lethal effects and impairment of repro-
duction” (Williams 1999, 26). American Cyanamid already has ob-
tained emergency permits to use the chemical in several states,
despite the fact that a laboratory study ordered by the EPA showed
that mallard ducks exposed to a level of the chemical said to be
typical of the wild laid 40 percent fewer eggs (which had a lower
hatching rate and birth rate) than a control group.
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6
End of the Line: The Dirty Dozen
and Human Health
Barbara Alice Mann, a friend and colleague, recalls:
I breast-fed Tassia [her daughter], which now makes me wonder whether

her allergies (and maybe, her diabetes!) are owing to that little act of mother-
love. Some of our health problems relate directly to our lack of certain an-
tigens in our blood (a Native American legacy, I hear), but the really weird
allergies we both have came from indiscriminate and irresponsible chemical
use by government and industry, I believe. I clearly remember walking home
from grade school—I was seven or so—while the city was spraying for pests.
I’m sure it was DDT. The truck came by, spewing out clouds of unbreathable
toxins, covering us little kids walking along the sidewalk, our papers and
books in hand. I remember coughing my way through the fog, indignant
because the guys operating the truck were laughing at having caught all us
little kids by surprise. However, I also recall an “infomercial” I saw later that
was being run on television concerning the spraying, at a time when the
nightly news was still revered as a truth-teller. The announcer said that the
spraying was safe for humans, and even showed people walking through
sprays with smiles on their faces. I now realize that this was the basest sort
of propaganda. I wonder about the extreme asthma I have now. At seven
years of age, however, I accepted the smiling faces in the chemical fog as
the gospel truth. (Mann, personal communication, December 9, 2000)
Mann, who lives in Toledo, Ohio, grew up a few years before

Rachel Carson’s Silent Spring (1962) first attacked “the myth of the
harmlessness of DDT” (21). Four decades later, each human deni-
zen of the Earth carries in his or her body residues of several hun-
dred dozen (or more) chemicals that were not present in the bodies
of our great-grandparents at the end of the nineteenth century. Be-
166 The Dirty Dozen
cause everyone now carries some of these chemicals, no unexposed

population exists to study as a control group.
Every child born today has been exposed to persistent organic
pollutants in the womb. Because these chemicals also become con-
centrated in breast milk because of their affinity for fatty sub-
stances, a baby may experience his or her most intense exposure to
POPs through breast-feeding. In nature, the breast-feeding of mam-
mals is merely one more step up a food chain that bioaccumulates
POPs.
Chemicals that were developed to control disease, increase food
production, and improve our standard of living have, in fact, become
a threat to biodiversity and human health. According to the World
Wildlife Fund, “This exposure threatens the integrity of the next
generation. Given these immense stakes, precaution dictates swift
and strong action to eliminate the use and production of persistent
chemicals. POPs by their nature cannot be managed” (World Wildlife
Fund 2000).
The toxic overload of POPs on the environment is not a small mat-
ter. The National Environmental Trust, Physicians for Social Re-
sponsibility, and the Learning Disabilities Association of America
have estimated that releases into the environment of developmental
and neurological toxins amount to about 24 billion pounds a year—
enough toxic chemicals to fill a line of railroad tanker cars stretch-
ing from New York City to Albuquerque, New Mexico. In many
places, old stockpiles of pesticides and industrial chemicals are an
increasing hazard to those who live nearby as they leak, leach, and
evaporate into the air from dumpsites and deteriorating storage
containers. Until effective and adequately funded disposal pro-
grams are put into place, new organochlorine emissions will con-
tinue to escape and add to the existing danger.
The health effects of these chemicals on human beings are sig-
nificant. Recent findings in human populations indicate that cer-
tain populations are most at risk, notably people who routinely
consume PCBs in fish and wildlife. According to one report, “These
susceptible populations include sport anglers, Native Americans,
women of child-bearing age, pregnant women, fetuses and nursing
infants of mothers who consume contaminated Great Lakes fish,
infants and children, the elderly, and the urban poor” (U.S. EPA
1996).
Neurobehavioral and developmental deficits occur in newborns
and continue through school-age children who have experienced in
End of the Line 167
utero exposure to PCBs. Other systemic effects, including liver dis-

ease and diabetes as well as compromises of the immune system,
may be associated with elevated serum levels of PCBs. Increased
cancer risks also have been associated with PCB exposures.
According to a study by the U.S. Environmental Protection
Agency,
Developmental effects [of PCB exposure] included a statistically significant

decrease in gestational age (by 4.9 days), birth weight (by 160 to 190 grams),
and head circumference (by 0.6 centimeters). Five months post-term these
effects were still evident compared to the control population. Neurobehav-
ioral deficits observed include depressed responsiveness throughout the
course of the study, impaired visual recognition, and poor short-term mem-
ory at seven months of age. At four years following birth, these deficits in
weight gain, depressed responsiveness, and reduced performance on the
visual recognition-memory test, one of the best validated tests for the as-
sessment of human cognitive function, were still evident. (U.S. EPA 1996)
According to the same study, “Adult men, women beyond repro-

ductive years, and the elderly are at an increased risk of cancer, and
may also be at an increased risk of immune and endocrine system
effects, from exposure to PCBs in fish.”
Boiled down to a small fistful of everyday English, these findings
send an electrifying message that everyone—even the cabinet mem-
bers of the George W. Bush presidency, who have pledged their sup-
port of the Stockholm Convention on POPs—can understand: Stop
the diffusion of POPs into the environment, and stop it soon, or
future generations face a wave of cancers and reproductive dis-
orders.
Several occupational or epidemiologic studies have indicated or
demonstrated other adverse health effects related to PCB exposure,
including cardiovascular, hepatic, immune, and musculo-skeletal
problems, as well as several types of cancers. Kreiss, Zack, and Kim-
brough (1981) reported a 30 percent increase over the national av-
erage in the incidence of hypertension in a PCB-exposed population
at Triana, Alabama. Kreiss and colleagues’ study associated in-
creased serum PCB levels with increased systolic and diastolic
blood pressure. Subjects’ PCB levels were elevated mainly because
they ate fish contaminated with the chemical.
Findings related to POPs have called into question the assump-
tion of pharmacology that dosage levels are the most important de-
terminant of toxicity. With some POPs, a low dose can induce more
168 The Dirty Dozen
of an impact than a high dose, a situation that scientists call a non-

monotonic response.
Researchers have linked organochlorine exposure to a wide vari-
ety of effects at different levels of exposure, including reproduc-
tive disorders (see chapter 7), malfunction of the nervous system,
diabetes, suppression of the immune system, disruption of the
endocrine system (thymus, thyroid, ovaries, testes, etc.), and repro-
ductive and developmental disorders. Specific conditions associ-
ated with PCB exposure include reduced fertility; intellectual and
attentional deficits; increased susceptibility to bacterial, viral, par-
asitic, and neoplastic disease; diminished intellectual, emotional,
and physical capabilities associated with hormonal imbalances;
and irreversible abnormalities of the brain, immune system, and
reproductive organs of offspring from pre- and postnatal exposures.
Average concentrations of dioxin now found among the populations
of the United States and Europe are at or near those levels associ-
ated with lower levels of testosterone, the hormone that influences
male sexual characteristics and the libido (sexual drive) in both men
and women; altered glucose tolerance, a symptom of diabetes; and
changes in the immune system (Allsopp, Costner, and Johnston
1995).
TOP OF THE FOOD CHAIN: THE PERILS OF

FISH CONSUMPTION
Bioaccumulation makes PCBs in fish especially hazardous to hu-
mans. Some PCBs persist in the body and remain biologically active
long after actual exposure ceases. In addition, a U.S. Environmental
Protection Agency report (1996) says, “Bioaccumulated PCBs ap-
pear to be more toxic than commercial PCBs and appear to be more
persistent in the body. For exposure through the food chain [there-
fore], risks can be higher than for other exposures.”
Some of the earliest investigations of PCBs’ effects on human pop-
ulations were conducted by Harold Humphrey of the Michigan De-
partment of Public Health and his colleagues. Their work, during
the 1970s and 1980s, demonstrated a correlation between levels of
PCBs in fetal tissues and maternal consumption of contaminated
fish (Humphrey 1983). The Michigan Maternal Infant Cohort Study
(Fein, Jacobson, and Jacobson 1984; Jacobson, Jacobson, and
Humphrey 1990; Jacobson, Fein, and Jacobson 1985) reported
End of the Line 169
both developmental disorders and cognitive deficits in the offspring

of mothers who ate contaminated fish six months prior to and dur-
ing pregnancy.
Schantz and colleagues (1996) studied sports anglers fifty to
ninety years of age, in two groups: high-volume fish eaters who con-
sumed twenty-four or more pounds of fish they caught in the Great
Lakes annually for more than fifteen years, and those who con-
sumed less than six pounds annually. This study demonstrated
that median levels of total PCBs, DDE, and mercury were signifi-
cantly higher in high-volume fish eaters than in low-volume fish
eaters. “The median serum total PCB concentration for high fish
eaters was 12 p.p.b. and 5 p.p.b. for low fisheaters; the maximum
values were 75 p.p.b. and 26 p.p.b., respectively. The median serum
DDE concentration for high fish eaters was 10 p.p.b. and 5 p.p.b.
for low fish eaters; maximum values were 145 p.p.b. and 33 p.p.b.,
respectively. . . . High-volume fish eaters [also] presented dispro-
portionately higher body burden levels of PCBs and DDE than low-
volume fish eaters in each decadal age group (i.e., 50–59, 60–69)”
(U.S. EPA 1996). Lonky and colleagues (1996) investigated new-
borns’ exposure to Great Lakes contaminants. Women in the high
fish-consumption group reported eating an average of 388 PCB-
equivalent pounds of Lake Ontario fish over sixteen years, which is
equivalent to about two pounds of salmon or lake trout per month.
Waller and colleagues (1996) conducted a similar investigation with
African-American women and their newborns.
Dellinger, Kmiecek, and Gerstenberger (1995) studied contami-
nants in the diets of Ojibwa who consume Great Lakes fish. Their
studies have associated elevated PCB serum concentrations with
self-reported diabetes and liver disease. This correlation confirms
similar findings of these investigators in the Red Cliff Band of Lake
Superior Ojibwa (between 1990 and 1993) (Dellinger, Kmiecek, and
Gerstenberger 1995).
Fitzgerald and colleagues (1996) studied a population of Native
Americans to investigate associations between consumption of lo-
cally caught fish and wildlife and body burdens of sixty-eight types
of PCBs, dichlorodiphenyl-dichloroethylene (DDE), mirex, and
hexachlorobenzene (HCB). Preliminary data from this study indi-
cated that Native American men who ate at least eight fish meals
per month for at least two years before participating in the study
had a mean PCB concentration of 5.4 ppb, which is higher than a
170 The Dirty Dozen
general population level of 1 to 2 ppb. Serum PCB level increased

with the number of fish consumed. The chemicals in question all
accumulated with age. Consumers of fish retained most of their PCB
burden, adding to it with each meal consumed.
POPS AND THE IMMUNE SYSTEM

Some organochlorine chemicals are toxic to the immune system,
reducing resistance to infection and tumors (Thomas 1990). Animal
studies indicate that many organochlorine compounds, including
PCBs, DDT, dieldrin, dioxins, hexachlorocyclohexane, hexachloro-
benzene, chlordane, and pentachlorophenol, are toxic to the im-
mune system (Safe 1994, 1995; Thomas 1990).
Studies of PCB exposure (Harada 1976; Hsu et al. 1985; Wong
and Huang 1981) via contaminated rice oil in Japan during 1968
and Taiwan in 1979 also contribute to the overall weight of evidence
that xenobiotic agents disrupt normal endocrine function and are
associated with neurobehavioral deficits. These incidents were re-
ferred to as yusho disease in the case of the Japanese studies and
yu-cheng disease in Taiwan.
Epidemiology studies following the yusho and yu-cheng incidents
in Japan and Taiwan, during which people ate rice contaminated
with PCBs and dioxins, showed significant reductions in some types
of immune system cells and an increase in respiratory bronchitis
and skin infections in exposed individuals. Similar results were ob-
tained in studies following a dioxin release in Times Beach, Mis-
souri, during 1983 that forced the abandonment of the town
(Allsopp, Costner, and Johnston 1995).
Following the PCB rice-oil contamination in Japan and Taiwan,
infants born of exposed mothers exhibited a range of neurobehav-
ioral problems. Cognitive testing “showed significantly lower overall
age-adjusted developmental scores in the exposed children” (U.S.
EPA 1996). Delays were observed at all age levels; they were greater
in children who were “smaller in size, had neonatal signs of intoxi-
cation and/or had a history of nail deformities” (U.S. EPA 1996).
Follow-up intelligence testing when the children were four to seven
years of age indicated that effects on cognitive development per-
sisted for several years following exposure (Chen, Guo, and Hsu
1992). These studies indicated that the presence of dibenzofurans
in contaminated rice oil (with PCBs) may have made the symptoms
End of the Line 171
worse. Furans were produced when the rice oil was heated prior to
human consumption.
POPS’ EFFECTS AND HIV/AIDS

Studies published during the 1990s raised a possibility that POPs
may act to suppress the immune system in ways similar to those of
the HIV/AIDS virus. The synergism of the human immunodeficiency
virus 1 (HIV-1) and dioxin on the immune system may be more del-
eterious than either by itself; both appear to have similar targets in
the immune system, causing suppression of certain lymphocyte
cells (T-cells) (Allsopp, Costner, and Johnston 1995). Comments
Joe Thornton, “The recent finding that the genome of the HIV-1 vi-
rus contains regulatory sequences that bind the dioxin-receptor
complex and activate transcription of viral genes is cause for con-
cern that dioxin-like chemicals may also play a role in the expres-
sion of infectious disease” (Yao et al. 1995, 366).
Dioxins, PCBs, and a number of other POPs undermine the im-
mune system by interfering with antibodies. Some organochlorines
(including PVC, PCBs, and some chlorinated solvents) “have been
associated with the development of autoimmunity, in which the im-
mune system attacks the body’s own tissues as foreign” (Thornton
2000, 62). Autoimmune diseases include lupus, rheumatoid ar-
thritis, and systemic sclerosis.
Human studies in Sweden and Canada have linked dietary intake
of PCBs and other POPs to immune system dysfunction. The Swed-
ish study noted a correlation between the level of PCBs, dioxins, and
furans in a given diet and significant reductions in the populations
of natural killer cells that play a key role in the body’s defenses
against cancer. Canadian researchers reported that children who
were exposed to high levels of POPs experienced rates of infection
ten to fifteen times higher than those of comparable, unexposed
children. A recent Dutch study exploring background levels of con-
taminants on children’s development linked immune system
changes in infants to their exposure to PCBs and dioxins before and
around the time of birth. The researchers noted that these problems
may presage such later difficulties as immune suppression, aller-
gies, and autoimmune diseases (World Wildlife Fund 2000).
In North Carolina, a group of infants was followed from birth to
examine the effects on the offspring of mothers with “normal” levels
172 The Dirty Dozen
(about 1 to 2 ppm) of PCBs in their bodies. Among 866 North Caro-

lina infants who were tested, higher PCBs in mother’s milk “was
correlated with hypotonicity (loss of muscle tone) and abnormally
weak reflexes. Subsequent studies of 802 North Carolina children
at ages six months and twelve months revealed those with higher
levels of PCBs had poorer performance on tests requiring fine motor
coordination” (Montague 1994). Researchers reviewing the history
of these children concluded, “There is thus consistent evidence that
prenatal exposure to levels of PCBs commonly encountered in the
U.S. produces detectable effects on motor maturation and some evi-
dence of impaired infant learning” (Tilson et al. 1990, 239).
ARE CANCER RATES RISING?

A National Cancer Institute report issued during 2000 states that
the incidence rate (the number of new cancer cases per 100,000
persons per year) for all cancers declined an average of 0.8 percent
per year between 1990 and 1997. “The greatest decrease in inci-
dence (at a rate of 1.3 percent per year) occurred after 1992,” ac-
cording to this report (Ries et al. 2000, 2398). This is not to imply,
says the report, that environmental carcinogens do not exist; mor-
tality rates also are down as a result of earlier detection and better
cancer treatments, making the level of cancer incidence a difficult
proxy for contamination of the environment.
The same report also concludes that “Breast cancer incidence
rates have shown little change in the 1990s, while breast cancer
death rates have declined about 2 percent per year since 1990 and
have dropped sharply since 1995” (Ries et al. 2000, 2398). “Inci-
dence and death rate for non-Hodgkins lymphoma among women
are continuing to increase, while incidence rates for melanoma for
both sexes combined have continued to rise about 3 percent an-
nually since 1981, [although] death rates have been approximately
level since 1989” (Ries et al. 2000, 2398).
Declines in general cancer rates may be masking, to some extent,
concurrent rises in cancers attributable to POP exposure. Rates of
some cancers have risen markedly. For example, according to Phil
Landrigan, a pediatrician and chairman of preventative medicine at
Mount Sinai School of Medicine, since 1972, the date at which na-
tional records began in the United States, the rate of brain cancer
incidence among children has increased 41 percent (Moyers 2001).
End of the Line 173
As Robert Napier commented in London’s Guardian:
Currently one person in three will get cancer and this figure will rise. The
idea that cancer is due to poor lifestyle, bad genes, or viruses is being in-
creasingly discredited. The massive increase in cancer in industrialized na-
tions is partially due to the release of 100,000 synthetic chemicals into the
environment, their concentration in the food chain, and their bioaccumu-
lation in humans. Each of us carries between 300 and 500 man-made
chemicals in our body. (Napier 2001, 19)
A seven-year study of breast cancer clusters on Long Island, con-

cluded during 2002, found no link with organochlorine compounds.
The Long Island Breast Cancer Study Project was one of the largest
and most comprehensive environmental epidemiologic studies of
possible association between environmental factors and breast can-
cer. The Long Island study was ordered by Congress in 1993 in re-
sponse to reports of elevated breast cancer deaths in a number of
northeastern states. The researchers looked at DDT and its metab-
olite DDE, chlordane, dieldrin, and PCBs.
According to a report by the Environment News Service, although
the study found no evidence that organochlorine compounds are
associated with the elevated rates of breast cancer on Long Island,
the researchers say that it is possible that breast cancer risk in
some individuals may be associated with organochlorine exposures
because of individual differences in metabolism and ability to repair
DNA damage. “Recent research by other investigators suggests that
organochlorine compounds may be related to the type of breast can-
cer that has clinical characteristics that are associated with de-
creased survival rates. This is an important issue that we are
continuing to investigate among the women in our study,” said prin-
cipal investigator Dr. Marilie Gammon, associate professor of epi-
demiology at the University of North Carolina at Chapel Hill School
of Public Health (Lazaroff 2002).
POPS AND CARCINOGENESIS

Regarding the carcinogenic nature of dioxins, Joe Thornton has
written,
Ironically, the most carcinogenic organochlorine is also the one whose car-
cinogenity is most controversial. TCDD (dioxin) is the most potent synthetic
carcinogen ever tested in the laboratory. There have been 18 separate as-
174 The Dirty Dozen
sessments of dioxin’s carcinogenicity, involving five different species of ex-

perimental animals, both sexes, five routes of exposure, and high and low
doses over short and long periods of time. In every case, dioxin has caused
cancer. (Thornton 2000, 190)
The carcinogenic properties of dioxins have been accepted as valid

science only since about 1990. Earlier than that, Monsanto, the
primary manufacturer of many dioxins, emphatically denied that
they caused cancer. As recently as the year 2000, the U.S. EPA was
debating whether dioxin was carcinogenic, at the same time that
the U.S. Army was giving a decoration (See chapter 1, “Agent
Orange”) to Vietnam veterans whose cancers could be traced to it.
Non-Hodgkin’s lymphoma has been one of the most rapidly in-
creasing malignant diseases in industrialized countries during the
last two decades. In epidemiologic studies, non-Hodgkin’s lym-
phoma has been associated with exposure to chemicals such as
phenoxyacetic acids, chlorophenols, dioxins, organic solvents (in-
cluding benzene), polychlorinated biphenyls, chlordanes, and im-
munosuppressive drugs. Levels of some types of dioxins and furans
were found to be significantly higher in the adipose tissue of seven
patients with malignant lymphoproliferative disease than in twelve
surgical controls without malignant disease. In addition, the Inter-
national Agency for Research on Cancer has established a strong
link between cancers and exposure to dioxin. Experimental evi-
dence and clinical observations indicate that these chemicals may
impair the immune system, which may be related to the fact that
risk for non-Hodgkins lymphoma increases in persons with ac-
quired and congenital immune deficiency as well as autoimmune
disorders (“Some Aspects” 1998).
POPS AND CHILDREN: SPECIAL

CONSIDERATIONS
Diazinon, one of the biggest-selling household pesticides in the
United States, during December 2000 was ordered banned by the
EPA in phases over a four-year period because of its health threats
to children. Diazinon is widely sold under such brand names as
Ortho, Spectracide, and Real-Kill. Diazinon is a member of the or-
ganophosphate family of chemicals, which attack the central ner-
vous system and can be especially toxic to children, even in low
doses. Retail sales for indoor use of the chemical have been ordered
End of the Line 175
to cease by December 2002; sales for outdoor use are to end by

December 2003. In December 2004 manufacturers will be obliged
to repurchase unsold retail supplies.
A report by the Center for Health, Environment, and Justice re-
vealed that nearly all Americans are exposed to unhealthy levels of
dioxins through normal daily consumption of food. This exposure
begins in the womb and continues through life. According to the
report, “America’s Choice: Children’s Health or Corporate Profit?”
children exposed to dioxins in utero during critical periods of devel-
opment appear to be the most sensitive and vulnerable to their toxic
effects. In children, dioxin exposure has been associated with low-
ered intelligence, increased prevalence of withdrawn and depressed
behavior, adverse effects related to an ability to focus attention, an
increase in hyperactive behavior, disrupted sexual development,
birth defects, and damage to the immune system.
About 20 percent of an average mother’s burden of fat-soluble
chemicals may be transferred to a newborn child during six months
of breast-feeding. Persistent organochlorines in a mother’s body
pass through the placenta to the embryo and fetus. Comment Ted
Schettler and colleagues, “Breast-feeding infants may get a dose of
dioxin, per kilogram of their body weight, within the first six months
of life that exceeds health-based limits . . . five times the allowable
daily intake of PCBs for a full-grown adult. Cow’s milk with levels
of PCBs this high would be too contaminated for sale in the United
States” (Schettler et al. 1999, 205).
Exposure to dioxins occurs over a lifetime, and the danger is cu-
mulative. Children’s dioxin intake is proportionally much higher
than adults’ because of the chemical’s presence in dairy products
and breast milk. Levels of exposure that cause no noticeable effects
in adults may cause irreversible harm to the developing fetus and
newborn (Thomas and Colborn 1992). Pre- and postnatal exposure
to persistent organochlorines may have profound effects in hu-
mans, among other animals. For example, lower birth weight,
slower postnatal growth, and reduced short-term memory have
been noted among the children of women who consumed moderate
amounts of organochlorine-contaminated fish from Lake Michigan
(Allsopp, Costner, and Johnston 1995; Jacobson and Jacobson
1990, 1993; Jacobson, Jacobson, and Humphrey 1990; Jacobson
et al. 1992).
An average nursing infant receives doses of dioxins and PCBs that
are twenty and fifty times higher than those of the average adult,
176 The Dirty Dozen
respectively (Thornton 2000, 42). In a year of nursing, an average

baby receives 4 to 12 percent of its total lifetime accumulation; be-
cause of bioaccumulation, this hypothetical infant will enter its sec-
ond year of life with the dioxin or PCB levels of a seventy-year-old
in the previous generation. These numbers are magnified again by
the high levels of contaminants in certain geographical areas, such
as the polar regions and higher elevations of mountain ranges. An
Inuit’s daily dose of dioxins, PCBs, toxaphene, and hexachloroben-
zene, for example, range from twice to forty-eight times the Cana-
dian government’s “tolerable daily intake” for adults (Thornton
2000, 42). Following dioxin contamination at Times Beach, Mis-
souri, during 1983, tests determined that children whose mothers
lived near dioxin-contaminated areas during their pregnancies had
abnormal brain function and altered immune systems. These ef-
fects, which were noted during early adolescence, are probably ir-
reversible (Smoger et al. 1993).
A study has assessed the association between persistent organ-
ochlorine compounds acquired via consumption of fatty fish from
the Baltic Sea (along the Swedish east coast) and infants’ lower-
than-normal birth weights. The study found that a mother’s high
current intake of fish from the Baltic Sea (at least four meals per
month) tended to increase the risk of having an infant with low birth
weight. Mothers who had grown up in a fishing village had an in-
creased risk of having an infant with low birth weight (Rylander,
Stromberg, and Hagmar 1996).
In utero exposure to polychlorinated biphenyls has been linked to
adverse effects on neurological and intellectual function in infants
and young children. Jacobson and Jacobson (1996) assessed these
effects through school age and examined their importance in the
acquisition of reading and mathematics skills. This study con-
cluded that in utero exposure to PCBs in concentrations slightly
higher than those in the general population can have a long-term
impact on intellectual function. Developmental toxins may interfere
with fetal development, sometimes causing birth defects. Neuro-
toxins can injure the developing brain, causing lifelong mental
impairment.
During the late 1990s, government health ministries in Denmark
and the Netherlands found that substantial amounts of phthalates
are released from PVC into human saliva. Dioxins, highly potent
synthetic hormone disrupters, are generated during the production
End of the Line 177
and disposal of PVC. This is important because a number of chil-

dren’s teething toys have been manufactured from flexible PVC
plastics. The governments of the Netherlands, Denmark, Belgium,
Austria, and Spain have sought bans on the use of soft PVCs in toys.
Some large toy retailers, including Toys-R-Us, removed these teeth-
ing rings from their stores shortly thereafter (World Wildlife Fund
2000).
A reexamination of 212 children from the Lake Michigan Maternal
Infant Cohort Study indicated neuro-developmental deficits as-
sessed in infancy and early childhood persisted at age eleven (Ja-
cobson and Jacobson 1996). These children were exposed in utero
through mothers who consumed fish six months prior to and during
pregnancy. After adjustment for a variety of potentially confounding
factors, study results indicated the most highly exposed children
(based on maternal milk PCB concentration) were three times as
likely to have low full-scale and verbal IQ scores. They also were
twice as likely to lag at least two years in reading comprehension.
Many also had difficulty paying attention. “These intellectual im-
pairments are attributed to in utero exposure to polychlorinated bi-
phenyls and to related contaminants at concentrations slightly
higher than those found in the general population” (U.S. EPA 1996).
The Lake Michigan study is striking not only because of the last-
ing impact seen in the children, but also because the fish-eating
mothers were not highly contaminated. The levels measured in their
bodies fall on the high end of what is considered the normal back-
ground range in the human population. The differences between the
levels in children and their mothers reflect the power of biomagni-
fication. The same study also is striking because it illustrates last-
ing impacts on the children.
In a similar U.S. study at the State University of New York (Os-
wego), researchers found measurable neurobehavioral deficits in
newborn children of women who had eaten the equivalent of forty
pounds of organochlorine-contaminated Lake Ontario salmon dur-
ing a lifetime. These children showed abnormal reflexes, a shorter
attention span, and an intolerance to stress. The Oswego study was
the first to document a wide range of effects on temperament stem-
ming from prenatal exposure to contaminants (World Wildlife Fund
2000).
A branch of the U.S. Public Health Service has concluded that
PCBs and dioxins are responsible at least in part for neurological
178 The Dirty Dozen
and behavioral deficits reported in children exposed in the womb.

This assessment by the Agency for Toxic Substances and Disease
Registry notes the “remarkable parallels” in the human epidemio-
logical evidence and corroboration from wildlife and laboratory evi-
dence: “The collective weight of the evidence indicates that certain
PCB/dioxin-like compounds found in fish . . . can cause neurobe-
havioral deficits. Further, these compounds have produced some
effects in some Great Lakes fish consumers” (World Wildlife Fund
2000).
A study in Mexico (Guillette et al. 1998, 347–53) reported striking
differences in the development of children exposed to agricultural
pesticides compared to children with minimal pesticide exposure.
In this study, researchers tested two groups of four- and five-year-
old children living in the Yaqui Valley region in northwestern Mex-
ico. The two groups were similar in all respects, including ethnicity
and diet, except for their exposure to pesticides. Families living in
the foothills are ranchers who rely almost exclusively on traditional
methods of pest control such as intercropping. The valley dwellers,
on the other hand, live in an agricultural area that has seen heavy
synthetic pesticide use since the 1940s.
Samples of human breast milk and cord blood taken from valley
women contained high levels of POPs that included several targeted
organochlorines: aldrin, endrin, dieldrin, heptachlor, and DDE. In
tests developed to measure growth and development, the pesticide-
exposed valley children fell far behind their foothill-dwelling peers.
Over a period of a few years, the valley children exhibited decreased
physical stamina in a jumping test, a lack of eye-hand coordination
evident in their decreased ability to catch a ball, diminished mem-
ory, and a notable inability to draw a sketch of a person, which is
used as a nonverbal measure of cognitive ability.
Louisiana and Texas emit more developmental and neurological
toxins to air and water than any other states. Tennessee, Ohio, Il-
linois, Georgia, Virginia, Michigan, Pennsylvania, and Florida also
are major emission sources (World Wildlife Fund 2000). “This is the
first complete snapshot we’ve ever had of toxic pollution in this
country that can affect the way that children’s bodies and brains
develop,” said Jeff Wise, policy director of the National Environmen-
tal Trust (Gordon 2000). Roughly 12 million U.S. children under
eighteen years of age (one out of every six) now suffer developmental,
learning, or behavioral disabilities, including mental retardation,
End of the Line 179
birth defects, autism, and attention-deficit hyperactivity disorder

(Gordon 2000).
“Now we know what we have suspected for years, that toxic chem-
icals are bringing anguish to thousands of families in this country,”
said Larry B. Silver president of the Learning Disabilities Associa-
tion of America and clinical professor of psychiatry at Georgetown
University Medical Center. “These are families that worry, work
overtime, and go without to take care of a child with a developmental
or neurological disability like mental retardation or learning dis-
abilities” (Gordon 2000).
This report (Gordon 2000) documents apparent increases in some
birth defects, attention-deficit disorder, and autism. The report also
compiles data describing increases in low birth-weight and pre-
mature births, both of which have been linked to effects of
endocrine-disrupting chemicals in animal studies.
“While it’s usually impossible to say that a particular child’s dis-
ability is caused by a toxic chemical, it is clear that toxic chemicals
are taking a tragic toll across the population,” said Ted Schettler,
an occupational and environmental health physician with Physi-
cians for Social Responsibility. “This report is yet another in a series
of wake-up calls to parents and policymakers that our children are
being harmed by the current chemical environment and lack of reg-
ulatory oversight” (Gordon 2000).
PCBS IN BREAST MILK

Research indicates that the breast milk of many women in all
parts of the world now contains levels of PCBs high enough to dam-
age a child’s immune system. Such babies are several times more
likely to contract chicken pox, middle-ear infections, and several
other illnesses. The same research contradicts previous assurances
by the British government, such as a comment by Sir Kenneth Cal-
man, then (in 1997) the government’s chief medical officer, who said
PCBs posed “negligible threats” to human health (Dennis and Leake
2000).
A study led by Nynke Weisglas-Kuperus, a pediatrician at Sophia
Children’s Hospital in Rotterdam, Holland, examined the develop-
ment of 207 babies born during the early 1990s. Half were breast-
fed and half given formula. Weisglas-Kuperus found that many of
the breast-fed babies received higher levels of PCBs than those fed
180 The Dirty Dozen
formula. All other factors being equal, breast-fed babies usually suf-
fer fewer illnesses than those who are bottle-fed, but high PCB levels
negated this benefit.
In the United States and most other industrialized countries,
PCBs are present in breast milk fat at about 1 ppm. An infant drink-
ing such milk will take in a quantity of PCBs five times the allowable
daily intake for an adult, according to standards established by the
World Health Organization (Thomas and Colborn 1992, 365). Chil-
dren exposed in the womb to PCBs at background levels in the
United States have experienced hypotonia (loss of muscle tone) and
hyporeflexia (weakened reflexes) at birth, delays in psychomotor de-
velopment at ages six and twelve months, and diminished visual
recognition memory at seven months (Tilson et al. 1990, 239).
Following cessation of commercial PCB production in the United
States during the 1970s, PCB concentrations in breast milk initially
declined. By the 1990s, however, PCB concentrations had generally
stopped falling (Furst, Furst, and Wilmers 1994). Although produc-
tion of many organochlorines in the United States has ceased, the
ecosphere’s burden of PCBs persists because quantities remain de-
posited in existing electrical equipment, in sediments, and in land-
fills and are still available for continued circulation throughout the
global environment.
PCBS AND SPONTANEOUS ABORTION

According to Rita Loch-Caruso of the Toxicology Program, De-
partment of Environmental and Industrial Health, University of
Michigan, some studies suggest that PCBs may disrupt the natural
termination of pregnancy by stimulating premature uterine con-
tractions. The cellular and molecular events underlying this toxicity
are unknown. Loch-Caruso and other researchers at the University
of Michigan have described a possible mechanism for PCB-induced
uterine contractions. In a series of experiments they discovered that
the PCB mixture aroclor 1242 can initiate cellular changes associ-
ated with contractions in uterine muscle cells.
Loch-Caruso contends that PCBs have been associated with
spontaneous abortion and shortened gestation length in women,
wildlife, and laboratory animals exposed to these industrial chem-
icals. Because premature birth is a considerable health problem in
the United States (it accounts for 75 percent of newborn deaths not
End of the Line 181
related to malformations), “it is important to determine how and to

what extent PCBs may disrupt normal uterine functioning. The
mechanistic understanding acquired in these studies is providing
much needed insight into reproductive risks that may arise from
PCB exposures” (Bae, Stuenkel, and Caruso 1999).
Increases in cancer mortality in workers exposed to PCBs have
been observed in several workplace studies (Bertazzi, Riboldi, and
Persatori 1987; Brown 1987; Sinks, Steele, and Smith1992; Yassi,
Tate, and Fish 1994). Elevated risks of malignant melanoma, gas-
trointestinal tract cancer, liver cancer, gall bladder cancer, biliary
tract cancer, and cancer of hematopoietic tissue have been reported
following PCB exposure. Kuratsune and colleagues (1988) reported
significant excess cancer of the liver by accidental ingestion of up
to two grams of PCBs two decades before the tests.
Exposure to organic solvents in general, including the organo-
chlorines tetrachloroethylene, trichloroethylene and 1,1,1-
trichloroethane, has been found to be significantly associated with
spontaneous abortion among female workers employed by in-
dustries using synthetic organochlorines. A study of Finnish
pharmaceutical-industry workers employed between 1973 and
1981 revealed that exposure to organic solvents, particularly meth-
ylene chloride, was associated with an increased risk of spontane-
ous abortion. For example, exposure to four or more solvents was
associated with a 350 percent increase in the risk of spontaneous
abortion, which was statistically significant, and exposure to meth-
ylene chloride was associated with a 230 percent increase in the
risk of spontaneous abortion, which had borderline significance.
Furthermore the risk increased with increasing frequency of expo-
sure to the solvents. The study also found an elevated risk for spon-
taneous abortion after exposure to estrogens when controlling for
the effects of other chemicals, although the number of women stud-
ied was small (Taskinen, Lindbohm, and Hemminki 1986).
DIETING DANGERS AND POPS

Researchers at Quebec City’s Université Laval have found that
weight loss may raise levels of PCBs and other pollutants in the
bodies of dieters. Pierre Ayotte and Eric Dewailly, who have studied
toxic organochlorine pollutants in the human body, joined with
Jonathan Chevrier, Pascale Mauriege, Jean-Pierre Despres, and
182 The Dirty Dozen
Angelo Tremblay to test what happens to body burdens of these

compounds when people lose weight. PCBs and other organochlo-
rine compounds stored in fat tissue release their toxicity into the
bloodstream as fat stores are dissolved. Such releases could cause
“a rise of these compounds in the heart, lungs, kidneys, liver and
spleen as well as brain” (Thompson 2001, A-3). These findings could
help to explain why obese people who have lost weight sometimes
have weakened immune systems and increased death rates.
“These results could possibly explain in part the controversial as-
sociation between weight loss and increased mortality rates,” the
researchers wrote. “Further studies are needed in order to assess
to what extent health complications and carcinomas could be trig-
gered by weight loss through such an increase in plasma (blood)
organochlorine concentrations” (Thompson 2001, A-3).
“It is far from clear that the increase we see after a weight loss
brings about health problems,” said Ayotte. He said that members
of the research team are divided on the question. “I don’t want peo-
ple to get the idea that it’s not good to lose weight” (Thompson 2001,
A-3). Ayotte said that the concentrations of the chemicals in most
Canadians are nowhere near the levels shown in populations such
as the Inuit, or in countries such as Mexico where pesticides such
as DDT are still in use. “To reach the levels found in the Inuit, a
person would have to lose 80 percent of the fat in their body,” Ayotte
said (Thompson 2001, A-3). Ayotte said that the study indicates that
Inuit who have ingested high levels of organochlorine compounds
might have to be more careful in losing weight.
In the Laval study, the first of its kind on humans, the researchers
followed thirty-nine obese individuals as they lost weight, testing
their fat tissue and blood for twenty-six organochlorine compounds
and compared them with a control group of fifty-seven average-
weight women. The researchers found an increase in nineteen of
the compounds studied, five of which increased significantly. Levels
of toxics tended to rise as more weight was lost by any one
individual.
THE PHYSIOLOGICAL DANGERS OF DIOXINS

Dioxins are among the deadliest and most pervasive of synthetic
chemical pollutants. Most dioxins are created by the application of
heat to the melting point of various organochlorine products during
End of the Line 183
several industrial processes, including the bleaching of most paper

pulp and the production of many pesticides. Many household plas-
tics (especially those containing PVCs) also release dioxins when
burned, so small-scale (often rural) trash burning by individual
households is a major source of these contaminants.
Exposure to dioxins and dioxin-like chemicals during fetal devel-
opment, infancy, and early childhood may be eroding the physical
and mental functions of current and future generations. Some of
the health effects linked to dioxins and dioxin-like chemicals in-
clude neurodevelopmental effects, such as reduced IQ, increase in
hyperactive behavior, adverse effects on attentional processes, in-
creased prevalence of withdrawn or depressed behavior; altered im-
mune function; central nervous system disorders; chloracne and
other skin disorders; disrupted liver and kidney function; altered
hormone levels, particularly thyroid, testosterone, and estrogen; re-
productive effects such as altered sex ratio, reduced fertility; en-
dometriosis; and liver, skin, and lung cancers (“Dioxin Deception”
2001).
A report by the EPA issued in 2000 concluded for the first time
that dioxins are human carcinogens. For the first time, the agency’s
draft report classified the most potent form of dioxin—2,3,7,8-
tetrachlorodibenzo-p-dioxin (TCDD)—as a human carcinogen, a
step above the previous ranking of probable carcinogen. More than
one hundred other dioxin-like compounds were classified as “likely”
human carcinogens (Skrzycki and Warrick 2000, A-1).
Environmentalists, extrapolating from the EPA’s risk findings,
have estimated that about one hundred of the roughly fourteen
hundred cancer deaths that occur daily in the United States are
attributable to dioxins (Skrzycki and Warrick 2000, A-1). These
findings came as a surprise even to EPA policymakers, who have
tracked slowly falling levels of dioxins in the environment, following
a series of tough new regulations on dioxin-emitting industries. The
EPA said that industrial emissions of dioxins were reduced roughly
80 percent between 1987 and 1995.
The EPA report noted that emissions of dioxins have plummeted
from their peak levels in the 1970s but still may pose a significant
cancer threat to some people who ingest the chemical through foods
in a normal diet. Standards for toxicity of dioxins (among other
POPs) have been dropping in recent years to the point where some
toxicologists believe that even residual amounts may have adverse
184 The Dirty Dozen
health effects, especially (as is the case in much of the world today),
because most people harbor some of these chemicals in their bodies.
Dioxins have been linked to several cancers in humans, including
lymphomas and lung cancer. The EPA report associates low-grade
exposure to dioxins with a wide array of other health problems, in-
cluding changes in hormone levels and developmental defects in
babies and children. For a small segment of the population who eat
large amounts of fatty foods, such as meats and dairy products that
are relatively high in dioxins, the odds of developing cancer could
be as high as one in 100, a risk ten times as high as the EPA’s
previous projections.
Dioxin is “the Darth Vader of toxic chemicals because it affects so
many systems [of the body],” said Richard Clapp, a cancer epide-
miologist at Boston University’s School of Public Health (Skrzycki
and Warrick 2000, A-1). During the last years of the 1990s, the U.S.
EPA imposed regulations on major dioxin emitters, including mu-
nicipal waste combustion, medical waste incinerators, hazardous
waste incinerators, cement kilns that burn hazardous waste, and
pulp and paper operations. When those regulations become fully
effective over the next few years, the agency expects further declines
of dioxin levels.
The production of dioxins permeates the manufacturing pro-
cesses of many common daily products. For example, chlorine
bleaching of pulp for paper products produces dioxins that can be
found in pulps, waste sludge, and other effluent. Incomplete com-
bustion during waste incineration, metals production, petroleum
refinement, and fossil fuel combustion are major sources of dioxins.
New methods in gas scrubbing and pulp bleaching have lowered the
amount of chlorine by-products produced over the years (Zook and
Rappe 1994).
TOLUENE AND DEVELOPMENTAL TOXICITY

More than 98 million pounds of toluene were released into the air
and water in the United States during 1998. The printing industry,
with many small to medium-sized facilities near residential areas,
is the largest source of air emissions of toluene, adding to the con-
cern about children’s exposure to this pollutant (Schettler 2000b).
Toluene can cause abnormalities of the face and head resembling
those of fetal alcohol syndrome, as well as growth retardation and
End of the Line 185
persistent deficits in cognition, speech, and motor skills. These de-

velopmental toxins may interfere with normal fetal development,
sometimes causing birth defects.
THE DANGERS OF LINDANE

Lindane (g-HCH, hexachlorocyclohexane) is included in the gov-
ernment Red List of dangerous substances. It has been in use as a
broad-range insecticide for fifty years, long enough to build up a
significant body of evidence on its toxic and environmental hazards.
The International Agency of Research on Cancer (IARC) has con-
cluded that lindane is a possible human carcinogen (class 2B). The
U.S. EPA has classified it similarly as a class B2/C possible human
carcinogen. The presence of lindane in human milk has been re-
ported in countries throughout the world.
Lindane has caused deaths and poisonings in humans and there
is authoritative recognition of its long-term health effects including
carcinogenesis. Scientific and anecdotal evidence links lindane with
serious health problems, including aplastic anemia, birth disor-
ders, and breast cancer (Pesticides Trust 1999). Included among the
reported chronic effects of exposure to lindane are nervous disor-
ders and increased liver weight.
Lindane is highly volatile. When it is applied to field crops, as
much as 90 percent of the pesticide enters the atmosphere and is
later deposited by rain. Lindane also leaches into surface and
ground waters. Like other organochlorine pesticides, lindane is fat-
soluble. This quality enhances its tendency to bioaccumulate along
food chains. Residues have been detected in the kidneys, liver, and
adipose tissue of a wide variety of wild animals and birds. It is highly
toxic to aquatic invertebrates and fish.
Lindane had been banned or severely restricted in thirty-seven
countries by 1999. The Advisory Committee on Pesticides in the
United Kingdom has so far carried out three reviews of lindane and
continued to recommend its approval. The Pesticides Trust believes
that Lindane should be banned on the basis of existing evidence
and as a precaution to avoid further health and environmental
problems that are suspected of being caused by lindane (Pesticides
Trust 1999).
Lindane is still widely used worldwide. It is commonly used as a
treatment for lice and scabies in humans and also against ectopar-
186 The Dirty Dozen
asites in animals. In a control study, Davis and colleagues (1993)

reported a statistically significant increase of brain cancer in chil-
dren following treatment with lindane shampoo. Veterinary use in
sheep can cause contamination of wool, as well as of milk and meat.
Several cases of human poisoning by lindane have been reported.
Children are significantly more susceptible than adults to the toxic
effects of lindane. In one case a dose equivalent to 62.5 milligrams
per kilogram proved fatal. In adults, doses above 300 milligrams per
kilogram ingested orally have proved fatal.
Lindane also works as an endocrine disrupter that is capable of
imitating hormones in humans and thereby disrupting the physi-
ological functions that these hormones control. A significant body
of evidence suggests that where lindane is used extensively, and
particularly where cattle are exposed to it, the incidence of breast
cancer rises. The United Kingdom has the highest rate of death from
breast cancer in the world, and in Lincolnshire were lindane is used
extensively on sugar-beet crops, the rate of breast cancer is 40 per-
cent higher than the national average (Pesticides Trust 1999). Ex-
posure to lindane also has been linked to blood dyscrasias as well
as aplastic anemia, in which formation of platelets and white cells
is disrupted (Pesticides Trust 1999).
AXING ATRAZINE
Chemicals used to enhance agricultural yields also may cause
problems with human health. During 1997, for example, the Envi-
ronmental Working Group (Casey and Hayes 1999) said that levels
of several herbicides, the most widely used of which is atrazine, were
too high in the tap water of 245 midwestern cities and towns. In
high doses, atrazine has been linked to several forms of cancer. In
the report, titled “Weedkillers by the Glass,” atrazine levels were said
to be highest in cities and towns throughout the Corn Belt (Indiana
westward to Nebraska) where atrazine is used liberally in surround-
ing agricultural areas. The report said that Omaha-area residents
who drink water drawn from the Platte River increase their lifetime
cancer risk by a factor of eleven. For those who drink water from
the Missouri River (Omaha uses both rivers), the lifetime cancer risk
is seven times the federal standard (Flanery 1994).
The makers of the chemicals protested. “The water is absolutely
safe,” said Chris Klose, speaking for the American Crop Protection
End of the Line 187
Association. “The [Environmental Working Group] study is without

scientific merit, and it’s damaging to the public trust” (Flanery
1994). The Environmental Working Group’s study found atrazine in
the drinking water of all the cities and towns tested in Nebraska and
Iowa—Omaha, Des Moines, Davenport, Cedar Rapids, and Iowa
City. The report recommended that parents in this area avoid ex-
posing infants and young children to tap water between May 1 and
August 30, when herbicide use on neighboring fields is most in-
tense. Parents were urged to use bottled water for infant formula
and frozen fruit juices. Donna Rhee, an environmental chemist in
Omaha, said that risks from atrazine and other herbicides include
breast cancer, gland cancer, and chromosome damage in animals
at levels that human beings have been ingesting (Thomas 1995).
UNINTENDED CONSEQUENCES OF WATER

CHLORINATION
Chlorine (hypochlorite) is added to drinking water in many coun-
tries as a disinfectant to prevent infectious diseases. It has proved
to be an enormously successful health-care measure, doubtlessly
preventing widespread illness and death. Chlorination of water may
provoke formation of several volatile organic chlorinated com-
pounds as the chlorine reacts with organic matter in the water. Most
of these by-products are called trihalomethanes (THM) and include
chloroform, which is known to cause cancer in animals (Allsopp,
Costner, and Johnston 1995; Cantor 1993; Zieler et al. 1988).
Evidence from several epidemiology studies has suggested an as-
sociation between chlorination of drinking water and an increased
risk of cancers of the bladder, colon, and rectum (Cantor 1993).
Which chlorinated by-products in water are responsible for the in-
creased risk of cancers is not yet clear. Recent animal studies have
suggested that the organic by-products of chlorination, namely
THMs, are of greatest concern (Dunnick and Melnick 1993). Evi-
dence also indicates, however, that the nonvolatile chlorinated by-
products are carcinogenic and are responsible for a major part of
the toxicity (Cantor 1993).
For individuals using chlorinated swimming pools, inhalation is
the main source of exposure, and since the chlorinated by-products
are volatile, particularly high exposures are experienced by those
who swim for a long time while exercising vigorously, which accel-
188 The Dirty Dozen
erates metabolism. Studies on competition swimmers using indoor

chlorinated swimming pools have found that chloroform levels were
elevated in their blood (Aiking et al. 1994).
CHLORPYRIFOS
Chlorpyrifos (better known under its trade name, Dursban) is a
key ingredient in a variety of products such as pet flea collars, ant
sprays, and, most notably, products designed for termite control.
Chlorpyrifos belongs to a class of thirty-seven persistent pesticides
known as organophosphates, which were initially developed as
nerve gases during World War II by the German chemical giant I.G.
Farben. Recent studies at Rutgers University indicate that chlor-
pyrifos persists much longer indoors than had been previously rec-
ognized. Carpets, soft furniture, and plush toys are especially likely
to absorb chlorpyrifos and to retain it for long periods of time as
vapors are released into the air.
Chlorpyrifos has been used widely for more than thirty years in
agriculture and in hundreds of products utilized by exterminators
and homeowners, including some Raid sprays, Hartz Yard and Ken-
nel Flea spray, and Black Flag Liquid Roach and Ant Killer. An EPA
assessment found that the chemical could damage the brain in new-
born rats and cause weakness, vomiting, diarrhea, and other ill ef-
fects in children.
Increased concern about chlorpyrifos emerged after studies—
some conducted by its manufacturer—were released showing that
the compound causes brain damage in fetal rats whose mothers
consumed the pesticide. The results of the animal tests are consid-
ered serious enough to indicate that the pesticide should not be
used where there are children, although the direct link to humans
is yet to be established.
The U.S. EPA has announced that products containing chlorpyr-
ifos will be phased out for home and garden use. The new rules allow
continued use of chlorpyrifos on many crops but sharply limit its
use on apples, grapes, and tomatoes. The new regulations also en-
tirely eliminate its use around homes, schools, day-care centers,
and other places where children may be exposed.
Restrictions on chlorpyrifos developed as part of the EPA’s reex-
amination of organophosphate pesticides. In 1999 the EPA banned
the use of pesticides with organophosphates and methyl parathion
End of the Line 189
on fruits and many vegetables and restricted the use of azinphos-

methyl. The Food Quality Protection Act of 1996 called for a much
stricter appraisal of chemical risks, focusing on potential harm to
children, whose small bodies and fast-growing brains are particu-
larly vulnerable to toxic chemicals (Revkin 2000).
Indian environmentalists during 2002 initiated a campaign for an
immediate ban on use of endosulfan, a pesticide that previously had
been outlawed in many parts of the world. The campaign followed
an Indian government report that linked use of endosulfan with dis-
ease and deformity, particularly of infants, in southern India. Ac-
cording to a report by the Environment News Service, activists of
the New Delhi–based group Centre for Science and Environment
(CSE) called for reinstatement of a former ban in the southern In-
dian state of Kerala (“Indian Enviros” 2002).
The CSE claimed to have obtained a copy of the report from un-
named sources in Kerala. The report found endosulfan residues in
water and blood samples collected from Padre, a village in northern
Kerala, in September and October 2001, ten months after the pes-
ticide had last been sprayed on the region’s cashew crops. The re-
port was said to have found a “significantly higher prevalence of
learning disabilities, low I.Q. and scholastic backwardness” among
children, as well as problems and congenital and reproductive ab-
normalities among people in the region. “It has also been found that
workers in the cashew plantations suffer from neurological prob-
lems such as trembling hands,” said Kushal Pandey, a reporter who
has been following the issue up for CSE’s environment magazine,
Down to Earth (“Indian Enviros” 2002).
MTBE: COMING TO A WATER TAP NEAR YOU

Human-created chemicals sometimes are introduced as solutions
to environmental problems, only to end up being problems them-
selves. Such has been the case with a common gasoline additive,
methyl tertiary butyl ether (MTBE), which has been used since
about 1990 to reduce the amount of pollution delivered to the at-
mosphere by automobiles burning gasoline.
The compound was never adequately tested before it was mar-
keted. When MTBE was enlisted in the war on automotive air pol-
lution, its effects on human health were unknown. The compound
helped clean the air, true enough. Only a few years after it began
190 The Dirty Dozen
leaking from thousands of faulty gasoline storage tanks around the

United States did anyone realize what it was doing to the water. By
the early 1990s, MTBE had become an important groundwater
contaminant.
MTBE, derived from natural gas, is added to gasoline in many
parts of the United States to reduce carbon monoxide and ozone
levels in the air (95 percent of total MTBE use), or to increase the
octane of gasoline (5 percent of use). MTBE is the most widely used
oxygenate for these purposes; however, ethanol is used in many
areas of the United States. Oxygenates such as MTBE and ethanol
reduce the need for benzene and other ozone-forming aromatic
compounds in gasoline.
MTBE, which was developed during the 1970s to replace lead as
an octane-booster for gasoline, is called an oxygenate because it
adds oxygen to gasoline. MTBE smells like turpentine and spreads
so quickly and evenly in an aquatic environment that a tablespoon
is more than enough to spoil the amount of water in an Olympic-
sized swimming pool. Even at five parts per billion, MTBE has a
distinct smell. MTBE is suspected of causing cancer in animals. (A
European study during the middle 1990s linked MTBE to liver and
kidney tumors in mice.)
In the South Tahoe Public Utility District, twelve of thirty-four
wells had been forced to close by early 2000 because of MTBE con-
tamination. “It’s a diabolical chemical. It moves up. It moves down.
It moves everywhere. Our feeling is that as long as MTBE is in gas-
oline, our groundwater is in jeopardy,” said Dennis Cocking of the
South Lake Tahoe Public Utility District (“Additive Poses” 2000).
During April 2002 a San Francisco jury determined that gasoline
containing MTBE is a defective product and that two major oil com-
panies knew about the problem when they began marketing fuels
containing the additive. The verdict, issued April 15, came in a
product-liability case filed by the South Lake Tahoe Public Utility
District over contamination of the district’s groundwater. According
to a report by the Environment News Service, MTBE had forced the
District to close one-third of its drinking-water wells by 1998, when
the utility filed suit (“Jury Labels” 2002).
According to the ENS account, “Lyondell Chemical Company, for-
merly Atlantic Richfield Chemical Company, Shell Oil Company,
and Tosco Corporation, now part of Phillips Petroleum, knew their
product was defective but withheld that information from the public
End of the Line 191
when they started selling gasoline boosted with methyl tertiary bu-
tyl ether (MTBE)” (“Jury Labels” 2002). This verdict is the first of its
kind, but dozens of similar cases have been filed by other utilities,
communities, and individuals across the country. In the next phase
of the trial, the jury will determine whether MTBE from the three oil
companies caused the groundwater pollution in South Lake Tahoe;
if the companies are found directly liable, damages will be assessed.
Santa Monica, California, also detected MTBE in its water supply.
By 2000 California (consumer of a tenth of the MTBE used in the
United States) had banned the substance within its borders after
2003. In the meantime, manufacturers of MTBE defended its use
as an environmental asset: “Because of cleaner-burning gasoline
with MTBE, cities like Los Angeles are enjoying their best air quality
in 50 years,” said Terry Wigglesworth, executive director of the Ox-
ygenated Fuels Association (“Additive Poses” 2000).
Paul Squillace, a U.S. Geological Survey research hydrologist,
said the detection of MTBE varied substantially among the thirteen
urban areas investigated. Urban areas where MTBE was most com-
monly detected included Denver (79 percent of wells), Harrisburg,
Pennsylvania (37 percent), and various cities in New England (37
percent). Urban areas where MTBE was not detected include Ocala
and Tampa, Florida, Portland, Oregon, and Virginia Beach, Virginia.
Possible sources of MTBE in groundwater include leaking storage
tanks and nonpoint sources such as recharge of precipitation and
stormwater runoff (Squillace, Pope, and Price 1995; U.S. Geological
Survey 1997). By contrast, only 1.3 percent of the wells sampled in
twenty agricultural areas had detectable concentrations of MTBE.
The U.S. Geological Survey said that none of the urban wells sam-
pled was being used as a source of drinking water. In general, public
water supplies draw from deeper groundwater, where MTBE con-
tamination is less likely.
The amount of MTBE released during refueling at service stations
and from engine exhaust is unknown, but it probably constitutes
an important source of MTBE contamination. Leaking underground
storage tanks and spills also may be sources of MTBE pollution.
Although MTBE will vaporize from soils, it can move into ground-
water. Once in groundwater, MTBE is more resistant to decay than
other gasoline components such as benzene (Snow and Zogorski
1995).
Ethanol (a gasoline-and-corn mixture widely used in the Ameri-
can Midwest) performs many of the same functions as MTBE but
192 The Dirty Dozen
costs more to produce. By the year 2000, some oil-industry leaders

were making the switch despite the cost, for environmental reasons.
Tosco, which owns Union 76 and Circle K stations, in December
2001 began to retool its refineries to utilize ethanol instead of MTBE.
“Ethanol is a renewable fuel with great environmental benefits, in-
cluding significant reductions in emissions of global warming
gasses,” said environmentalist Elisa Lynch of the Bluewater Net-
work (Gardner 2000). “Farmers and the entire state would benefit
from converting biomass to renewable fuel while we’re addressing
the concerns of how to dispose of agricultural wastes,” said Jack
King, national affairs manager for the California Farm Bureau
(Gardner 2000).
Shell Oil Company during August 2002, agreed to pay $28 million
to settle a lawsuit over MTBE contamination of wells in the South
Tahoe Public Utility District. Pollution with MTBE had forced the
South Lake Tahoe District to close one-third of its drinking-water
wells by 1998, when the utility filed suit. The South Lake Tahoe
Public Utility District also has settled with Chevron, Exxon, and
others, and is expected, with the Shell settlement, to receive more
than $69 million from refiners for cleanup and legal costs (“Shell
Will Pay” 2002).
In April 2002, a California jury decided that gasoline containing
MTBE is a “defective product,” and that Shell, Lyondell Chemical
Company, and Tosco Corporation knew about the problem and
withheld information from the public when they began marketing
fuels containing MTBE. During July 2002, MTBE manufacturer
Lyondell agreed to pay $4 million to settle its role in the South Lake
Tahoe case. Before the case went to trial, Exxon settled for $12 mil-
lion and Chevron settled for $10 million (“Shell Will Pay” 2002).
The settlements could set a precedent for similar cases now being
tried in other states across the nation. At least sixteen states have
reported water contamination due to MTBE. According to the En-
vironment News Service, California Governor Gray Davis has issued
a ban on the use of MTBE in all fuel sold within the state, effective
January 2004. At least three oil companies (Atlantic Richfield,
Exxon, and Shell) have said that they plan to stop boosting their
gasoline with MTBE before that deadline (“Shell Will Pay” 2002).
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7
Toxic Barbie? Not Your Great-
Grandmother’s Estrogen
The density and abundance of sperm required to maintain the fe-

cundity of the human animal is open to dispute; at some point, how-
ever, damage to sperm counts, taken far enough, must inhibit
reproduction. Comes now the most intriguing question of our jour-
ney into the endocrine-disrupting potential of POPs: Has human-
kind’s ingenuity—notably our products’ dexterity in mimicking
estrogen—planted the seeds of an eventual reduction in human-
kind’s population? And what could such an outcome do to many a
cherished assumption of the early twenty-first century, with in-
creasing numbers of human beings crowded onto an Earth beset by
an overload of greenhouse gases and other forms of human-induced
pollution?
Eventually, perhaps, a cold wind may blow through the halls of
human artifice. Amid humanity’s festival of fecundity now come
warnings that synthetic chemicals may prejudice the reproductive
systems of many animals, including human beings. One report
commented, “This is of great concern because effects on the next
generation, and especially disturbances of the reproductive system,
rapidly threaten populations as a whole” (Allsopp, Costner, and
Johnston 1995).
We come now to the era of competing anthropogenic ecological
holocausts. For example, could the endocrine disrupters in many
man-made chemicals cause human sperm counts to fall so low that
the human race will eventually find its gene pool in peril? Such a
future could certainly (if eventually) stabilize the atmosphere’s over-
load of greenhouse gases, for example. The endocrine-disrupting
qualities of many organochlorines pose one of the fundamental iro-
200 The Dirty Dozen
nies of global pollution. Has the ingenuity of the chemical industry

created products that will ultimately render sterile at least some
portions of the human race? Eventually, could the human race, au-
thor of so many plant and animal extinctions because of its prolific
breeding and expropriation of the Earth’s resources, itself become
a victim of human artifice?
H. Burlington and V. F. Lindeman were the first, in 1950, to sug-
gest that DDT might mimic estrogen, “because of its inhibition of
male characters in developing cockerels” (Jefferies 1975, 193, 224).
Burlington and Lindeman used seventy male chicks (thirty controls
and forty experimental animals) to investigate the developmental
effects of DDT. The experimental animals were injected with purified
DDT in a solvent of chicken fat; the control animals were injected
with chicken fat alone. According to Sheldon Krimsky, “The results
were striking. The experimental animals had smaller testes and
showed arrested development of secondary sex characteristics,
compared with the controls” (Krimsky 1999, 6).
Colborn and colleagues have argued that
Evidence already exists that a number of organochlorine chemicals (such
as dioxin, PCBs, and DDT) have reached concentrations in aquatic food
sources that can lead to substantial functional deficits in animals that con-
sume this food. . . . Based on current breast-milk concentrations nation-
wide, it is estimated that at least 5 percent and possibly more of the babies
born in the United States are exposed to quantities of PCBs sufficient to
cause neurological effects. (Colborn, vom Saal, and Soto 1993, 378)
As of this writing, however, any prospective, notable decline in

human numbers remains a matter of speculation. During the year
2000 on the Christian calendar, half the human beings who ever
had lived were alive, six billion people. Extinction of the human race
does not seem to be a pressing issue, given our inundation of the
world with increasing tides of humanity. At the same time, some
estimates of male sperm counts have declined by half in the United
States and other parts of the world during the half century since
DDT and other synthetic organochlorines were first introduced into
the environment (Sharpe 1993).
We may be skewing the natural order of reproduction by bathing
the biosphere in synthetic estrogens. By the middle 1990s, at least
51 synthetic chemicals had been detected that disrupt the endo-
crine system in some way (Colborn, Dumanoski, and Myers 1996,
81). Some, like DES, mimic natural estrogen, while others interfere
Toxic Barbie? 201
with testosterone, thyroid metabolism, or other parts of the system.

This list of endocrine disrupters includes (as one of the 51 previ-
ously mentioned) the 209 different compounds that are classed as
PCBs, 75 dioxins, and 135 furans (Colborn, Dumanoski, and Myers
1996, 81).
During April 1997 the European Environment Agency published
a report on a major conference on endocrine-disrupting chemicals
held December 2–4, 1996, in Weybridge, England. The Weybridge
Report concluded
It is evident that there are adverse health trends affecting the reproductive
organs of both men and women. Thus, the incidence of testicular cancer
has increased quite dramatically in countries with cancer registries, in-
cluding Scandinavia, the countries around the Baltic Sea, Germany, United
Kingdom, United States of America, and New Zealand. Similarly, there has
been an increase in the incidence of breast cancer in many countries and
the incidence of prostate cancer also appears to have risen. (European Work-
shop 1997, part 1, 6)
While improved reporting may be responsible for some of the in-

creases, problems related to endocrine-disrupting chemicals can-
not be excused entirely. Furthermore, according to the Weybridge
Report, the apparent decline in male sperm counts in some coun-
tries “is likely to be genuine, and not attributable to confounding
factors or methodological variables” (European Workshop 1997, part
1, 6). The same report cited “insufficient evidence to definitely es-
tablish a causal link” between the health effects seen in humans
and exposure to chemicals (European Workshop 1997, part 1, 6).
Concern and further investigation are warranted, however, accord-
ing to the report (part 1, 14).
POPs had contaminated the environment by the time scientists
discovered that many of them mimic the female hormone estrogen,
and thereby disrupt reproduction, specially in animals (such as hu-
mans) who reside at the top (or end) of their respective food chains.
Describing these “endocrine disrupters.” Pat Costner observed
The body’s hormone system, also known as the endocrine system, is a com-
plex internal chemical messenger system, which regulates vital functions
such as our reproductive systems, behavior, and immune systems. In par-
ticular, the hormone system controls the development of these vital func-
tions in the unborn child. Hormones are produced by a variety of glands in
different parts of the body and released into the blood stream. The hor-
mones bind to special receptors in organs or tissues and cause them to
202 The Dirty Dozen
respond in a specific way. Hormones are extremely powerful, having effects

at levels of only parts per trillion. But in our bodies, concentrations of hor-
mones are strictly controlled. (Costner 1997)
During 1993 the U.S. federal government’s National Institute of

Environmental Health Sciences in Bethesda, Maryland, published
a report describing the developmental effects of synthetic chemicals
on humans and animals that occur in the womb or the ovum. Theo
Colborn was the primary author of this report, which considered
the following endocrine-disrupting chemicals: 2,4,-D, 2,4,5-T,
alachlor, amitrole, atrazine, metribuzin, nitrofen, trifluralin, beno-
myl, hexachlorobenzene, mancozeb, maneb, metiram-complex, tri-
butyl tin, zinab, ziram, beta-HCH, carbaryl, chlordane, dicofol,
dieldrin, DDT and metabolites, endosulfan, heptachlor and hep-
tachlor epoxide, lindane (gamma-HCH), methomyl, methoxychlor,
mirex, oxychlordane, parathion, synthetic pyrethroids, toxaphene,
transnonachlor, aldicarb, DBCP, cadmium, dioxin (2,3,7,8-TCDD),
lead, mercury, PBBs, PCBs, pentachlorophenol (PCP), penta- to
nonylphenols, phthalates, and styrenes.
According to this report, “Damage occurs in three key bodily sys-
tems: the reproductive system, the endocrine system, and the im-
mune system” (Montague 1993). The endocrine system comprises
specialized cells, tissues, and organs that create and secrete hor-
mones, usually into the blood), which then regulate other cells. Hor-
mones thus act as messengers, “sending chemical signals that
control the way the entire body grows, is organized, and behaves”
(Montague 1993). Colborn, vom Saal, and Soto (1993) describe how
endocrine-disrupting chemicals mimic hormones, with one key dif-
ference. Natural hormones do their work as messengers,
and then the body disassembles [natural hormones] and removes them
from the blood stream. In contrast, when industrial chemicals and pesti-
cides mimic hormones, they do not disappear quickly. They tend to remain
in the body for very long periods, doing the work of hormones at times, and
in ways, that are inappropriate and destructive. . . . Effects of exposure
during development are permanent and irreversible. (378)
Development of the male reproductive tract during fetal life in hu-

mans is very sensitive to levels of estrogen. Higher-than-usual es-
trogen levels may have a role in reducing sperm counts. Chemicals
that mimic the effects of estrogen in the body may cause the femi-
nization of many exposed males (Sharpe 1993, 357).
Toxic Barbie? 203
Organochlorines cause specific responses that are usually trig-

gered only by natural estrogens. Estrogenic chemicals also may al-
ter estrogen metabolism by modulating the number of estrogen
hormone receptors and their binding affinities. Estrogens play a
crucial role in controlling reproduction in women and to a lesser
extent in men; they also are involved in fetal development. There-
fore, interference by exogenous estrogens can have far-reaching ef-
fects on the body (Allsopp, Costner, and Johnston 1995).
Because many disorders of reproductive system have a common
origin in fetal life or childhood and most do not become evident until
adulthood, the increase in disorders seen today probably originated
twenty to forty years ago. The prevalence of such defects in male
babies born today, at today’s levels of contamination, will therefore
not become manifest for another twenty to forty years (Danish EPA
1995).
FALLING SPERM COUNTS

During the last thirty to fifty years disorders in men related to
reproductive organs have risen sharply in several countries. Such
disorders include declines in sperm count, according to some stud-
ies (e.g., Carlsen et al. 1992) totaling 50 percent during fifty years.
The fact that these fifty years (1945–1995) coincide with the advent
and worldwide diffusion of synthetic organochlorines may be no co-
incidence. A study by Elkington (1985) indicated that American men
during the 1980s produced half the sperm they did fifty years ear-
lier. Addressing causation, “the research strongly suspects . . . the
increased use of herbicides, pesticides, and a chemical flame retar-
dant used in foam mattresses” (Hynes 1989, 22).
Niels Skakkebaek, a pediatrician at the National University Hos-
pital in Copenhagen (where he directs the Department of Growth
and Reproduction), discovered the dramatic fall in sperm counts
while he was seeking an explanation for unusually high rates of
testicular cancer in Danish men. His work led him to study world-
wide reports of sperm counts. Skakkebaek studied sixty-one
sperm-count reports in twenty-one countries throughout North
America, South America, and Asia. Their summary showed a de-
crease in mean sperm count from 113 million per milliliter in 1940
to 66 million per milliliter in 1990. Skakkebaek (1972) and Sharpe
(1993) attributed the decline at least in part to estrogenic organ-
ochlorines.
204 The Dirty Dozen
While Skakkebaek’s work has been debated, it also has been sup-
ported by other researchers. In 1992, for example, E. Carlsen and
colleagues (1992) published an analysis of studies of male sperm
counts, a summary of studies from various nations with data on
almost 15,000 men. Results indicated a large drop in the mean
sperm count of 42 percent between 1940 and 1990. This study has
been criticized because sperm counts rose slightly after most of the
studies documented by Carlsen were conducted. During the 1990s,
however, new studies revealed that sperm counts again were gen-
erally declining (Auger et al. 1995; Irvine 1994). In addition, a study
published in the British Medical Journal (Stewart et al. 1996) re-
ported a 24 percent decline in motive (actively swimming) sperm in
Scottish men born during the 1950s. The study indicated as well
that men born later tended to have lower sperm counts.
Medical researchers’ published reports of dramatic declines in
sperm counts and increasing sperm abnormalities over the past
half century have caused a contentious debate over whether these
changes are related to organochlorines. Two of Europe’s leading re-
productive researchers have hypothesized that increasing exposure
to environmental estrogens, which include several POPs, is likely to
be responsible not only for lowered sperm counts but also for genital
defects, testicular cancer, and other male reproductive abnormali-
ties. Animal studies have also made it clear that humans are cur-
rently exposed to levels of dioxins that are roughly equivalent to
levels that have caused significant sperm-count declines in male
rats exposed in the womb. As researchers probe the cause of the
reported human sperm-count declines and other male reproductive
problems, POPs stand high on the list of suspects.
SPERM COUNTS AND AGRICULTURAL

CHEMICALS
Researchers during 2002 published findings indicating that se-
men quality differs significantly between regions of the United
States in patterns suggesting that fertile men in more rural areas
have lower sperm counts and less vigorous sperm than men in ur-
ban areas. The researchers associated environmental factors, such
as extensive use of agricultural chemicals, to these differences. Fer-
tile men in Missouri’s rural Boone County were found to have a
mean sperm count of about 59 million per millimeter, compared to
Toxic Barbie? 205
103 million for men in New York City, 99 million in Minneapolis,

and 81 million in Los Angeles. The sperm of men in Boone County
were not only less numerous; they also were less vigorous, accord-
ing to the study (“Rural Men” 2002, A-11; Swan et al. 2002).
Dr. Shanna Swan, an epidemiologist and research professor of
Family and Community Medicine at the University of Missouri–
Columbia, led a group of researchers who studied 512 couples
receiving prenatal care at clinics in Columbia; Minneapolis, Min-
nesota; Los Angeles, California; and New York, New York. They
found that semen quality was equally high in Minneapolis and New
York, and slightly lower in Los Angeles. However, men in mid-
Missouri had counts and quality that were significantly lower—
slightly more than half—than that of men from any of the urban
centers. The study appeared in the November 11, 2002, online edi-
tion of Environmental Health Perspectives, a scientific journal pub-
lished by the National Institute of Environmental Health Sciences.
“We believe that agricultural chemicals could be contributing to this
decrease in semen quality,” Swan said. “The county in which our
Missouri participants lived is quite rural. In 1997, 57 percent of the
land was used for farming, compared to 0 to 19 percent for the other
three [urban] counties we studied. We are continuing this research
and examining the exposure of men to specific chemicals used in
farming” (“Chemical Exposure” 2002; Swan et al. 2002). According
to an account by the Environment News Service (“Chemical Expo-
sure,” 2002), “The only other published study on a comparable
semi-rural population analyzed semen quality among men in Iowa
City, and also found reduced sperm concentration. Swan and her
colleagues are now studying semen quality in Iowa City.”
MALE SEXUAL DYSFUNCTION

In addition to falling sperm counts, measures of several other
male sexual dysfunctions rose sharply during the closing decades
of the twentieth century. Incidence of testicular cancer in men un-
der age thirty-four has been increasing rapidly in many countries.
Recent studies suggest this cancer in young men arises from events
early in life or even in the womb, as evidenced by the higher rates
of testicular cancer among men with developmental defects such as
hypospadias (incomplete masculinization of the male genitals) and
undescended testicles.
206 The Dirty Dozen
In the United States, young men fifteen to thirty years of age ex-
perienced a 68 percent rise in the rate of testicular cancer between
1972 and 2000 (Moyers 2001). Between 1962 and 1981 the fre-
quency of undescended testicles doubled in England and Wales. The
rate of hypospadias in the United States doubled in male infants
during the last quarter of the twentieth century (Chilvers, Pike, and
Foreman 1984; Jackson, Chilvers, and Pike 1986; Paulozzi, Erick-
son, and Jackson 1997). Similar increases were reported at the
same time in several European countries and Japan. Hypospadias
also has been reported when human males were exposed prenatally
to antiandrogens such as DDE, a by-product of DDT’s breakdown
(World Wildlife Fund 2000).
During development of the human fetus, hormones orchestrate
key events such as sexual differentiation and the construction of
the brain, and so synthetic chemicals that interfere with hormone
messages, including each one of the dirty dozen, can disrupt devel-
opment and cause lifelong damage. In one study of dioxins, reported
by the U.S. National Academy of Sciences (2000), a human fetus
tested as being 100 times as sensitive as an adult. In the same re-
port, a single low dose of dioxin administered to a pregnant rat at a
critical moment in pregnancy did permanent damage to the repro-
ductive systems of her pups, which showed notably diminished
male sexual behavior and a sperm-count drop of as much as 40
percent. The dose was very close to the levels of dioxins and related
compounds generally reported in people in industrialized regions
such as Europe, Japan, and the United States. In female fetuses,
the most vulnerable organs are the breasts, fallopian tubes, uterus,
cervix, and vagina. In male fetuses, the critical organs are prostate,
seminal vesicles (where sperm originates), epididymides (reservoirs
for sperm), and testicles. In both sexes, critical organs are the ex-
ternal genitals, the brain, skeleton, thyroid, liver, kidney, and im-
mune system.
Other disorders of the male reproductive system also have in-
creased. Testicular germ-cell cancer is now the most common ma-
lignancy among young men in many industrialized countries. The
Danish Cancer Registry has collected reliable data since 1943 on
the incidence of testicular germ-cell cancer showing a three- to four-
fold increase between the 1940s and 1980s. Studies based on data
from cancer registries in other countries, including the United King-
dom, the Scandinavian and Baltic countries, Australia, New Zea-
Toxic Barbie? 207
land, and the United States also have reported significant increases
in the incidence of testicular cancer.
THE YUCHENG INCIDENT AND DECLINING

SPERM COUNTS
A large number of Taiwanese were poisoned during 1978 and
1979 in the Yucheng Incident as they consumed PCB- and dioxin-
contaminated rice that had been cooked with polluted oil. The rice
oil contained 100 ppm PCBs and 0.1 ppm PCDFs [polychlorinated
dibenzofurans]. Two studies describing the sexual development of
children born to women who were pregnant at that time (Guo, Chen,
et al. 1994; Guo, Lai, et al. 1993) revealed that penis sizes of boys
born seven to twelve years after the poisoning were significantly
shorter than the penises of matched control children. The penises
were probably stunted because of in utero exposure to estrogenic
PCBs (Holloway 1994, 25). Roughly 2,000 people consumed the
contaminated oil. The children consumed no contaminated oil
themselves; they were exposed before birth to PCBs that were car-
ried by their mothers’ milk (Montague 1994; Rogan et al. 1988, 334).
The Yucheng or “oil disease” children were followed medically for
several years. When 115 Yucheng children were examined in 1985,
they were less developed than a control group of children on thirty-
two of thirty-three measures. Compared to controls, they were de-
layed in the age that they performed tasks such as saying phrases
and sentences, turning pages, carrying out requests, pointing to
body parts, holding pencils, and catching a ball. The Yucheng chil-
dren also had a variety of physical defects at birth, including dark-
colored heads, faces, and genitals, and abnormal nails that were
often dark and ridged, split, or folded (Kolata 1988; Montague
1994). These children provided the first direct evidence that PCBs
produce birth defects—that they are, in medical terminology,
teratogenic.
INFERTILITY AND DBCP

Other organochlorine pesticides, such as dibromochloropropane
(DBCP), have caused infertility in men who have been exposed to
the compound at their work sites (Whorton and Foliart 1983). DBCP
was used as a soil fumigant beginning in the mid-1950s; its use
208 The Dirty Dozen
peaked during the mid-1970s, before disclosures of infertility pro-

voked the U.S. EPA to ban its manufacture and use in 1979.
The first indication that DBCP caused infertility in men arose in
1977, when a group of five male workers at a California pesticide
formulation plant sought medical advice after talking among them-
selves about their shared inability to father children. All five were
found to have low sperm counts. Further investigation at the plant
produced a very strong relationship between the duration of DBCP
exposure and sperm-count decline. According to one observer, “The
exact mechanisms by which DBCP exerts adverse effects on the
male reproductive system are unknown, but it is clear that it dam-
ages and destroys the germ cells that produce sperm. This results
in a reduction in the numbers and motility of sperm that causes
infertility. Sperm counts have recovered in some of the men affected
by DBCP, but others remain sterile” (Allsopp, Costner, and John-
ston 1995).
Large amounts of DBCP were used in the Atlantic banana-
growing regions of Costa Rica between 1971 and 1978. Workers
were typically exposed to the chemical for long periods of time. By
mid-1990, approximately 1,500 male workers from these banana
plantations were diagnosed as infertile. Physicians on the scene es-
timated that about a thousand similar cases had not been reported.
Between 60 and 70 percent of all sterile victims were azoospermic
(having no sperm to count) and the rest are oligospermic (having
low sperm counts of less than 20 million per milliliter). Since virility
is often accorded a high social value among men in Latin America,
its loss due to DBCP toxicity provoked other psychological and so-
cial effects, including depression (in more than half the patients),
impotence, and an increasing number of divorces attributable, at
least in part, to DBCP-induced sterility (Thrupp 1991).
Dioxins have displayed adverse effects on male reproductive sys-
tems in animals and humans from birth to death. Experiments on
rats and other laboratory animals have shown that exposure of
adult males to high levels of dioxins produces changes in the levels
of male reproductive hormones, including a reduction in testoster-
one, decreased sperm formation (and fertility), as well as reduced
weights of the testis (Peterson, Theobald, and Kimmel 1993). During
the Vietnam War, dioxin-contaminated Agent Orange was sprayed
liberally in Southeast Asia by U.S. armed forces (see chapter 1).
Members of the U.S. armed forces who sprayed Agent Orange often
Toxic Barbie? 209
were contaminated with dioxins. Some of these men’s testes shrank

after exposure, an effect that has been linked by Wolfe, Michalek,
and Miner (1994) to dioxin contamination.
SYNTHETIC ESTROGEN AND BREAST CANCER

The incidence of breast cancer has steadily risen worldwide. By
the 1990s, it was the leading cause of death from cancer for women
in the United States (El-Bayoumy 1992). Breast cancer mortality
has increased at an estimated rate of 1 percent per year since the
1940s in the United States, even allowing for increased detection
rates by mammography. Between 1982 and 1986, breast-cancer
mortality rose by 4 percent a year. Increases have occurred in all
age groups (Harris et al. 1992).
Because synthetic estrogenic chemicals in the environment can
mimic natural endogenous estrogens or interfere with their metab-
olism, it has been hypothesized that such chemicals may increase
the risk of breast cancer (Davis et al. 1993). A number of organo-
chlorine compounds (DDT and symmetrical triazine herbicides
such as simazine chlortriazine and Atrazine) have been shown to
induce and promote breast cancer in laboratory animals (Stevens
et al. 1994; Wetzel et al. 1994). Increased concentrations of estro-
gens during pregnancy also may increase the risk of breast cancer
in daughters (Trichopoulos 1990). According to expert testimony,
“There is considerable evidence that the total lifetime exposure to
estrogen influences the likelihood of developing breast cancer. High
serum or urine levels of estrogen, early onset of menstruation, de-
layed menopause, and delayed first-child bearing are all risk factors
for breast cancer” (Schettler et al. 1999, 160). Risk factors also in-
clude radiation exposure and alcohol consumption.
The rising level of synthetic estrogens in the environment may not
be the single cause of rising breast-cancer rates during the last half
of the twentieth century, but one factor among many that influence
lifetime exposure. Commented Schettler and colleagues (1999), “A
considerable amount of interest and research is focussed on . . .
organochlorine compounds, solvents, metals, and polycyclic aro-
matic hydrocarbons, which are products of combustion spread
widely throughout the environment. Breast milk contains a large
number of these contaminants in complex mixtures” (Schettler et
al. 1999, 160).
210 The Dirty Dozen
Because of breast cancer’s complex origins, scientists have had

trouble tracing singular causes. Given that caveat, breast-cancer
rates have risen substantially during the time that POPs have be-
come pervasive in the environment. During the middle 1940s, one
in twenty-two women was afflicted with breast cancer at some
point in her lifetime. By the end of the 1980s, that ratio was roughly
one in eight (Cadbury 1997, 220). Some of this rise may be due to
increased detection and treatment of the disease. The rest of the
increase defies singular or simple explanation.
A link between estrogenic chemicals and cancer was suspected
as early as the 1930s by E. C. Dodds and colleagues (Dodds, Gold-
berg, and Lawson 1938; Dodds et al. 1938; Dodds and Lawson
1938). A. P. Høyer and colleagues (1998) showed that women, once
afflicted by breast cancer, do not survive as long if they have rela-
tively high levels of dieldrin in their blood.
Dieldrin had a significant adverse effect on overall survival and breast can-
cer specific survival . . . These findings suggest that past exposure to estro-
genic organochlorines such as dieldrin may not only affect the risk of
developing breast cancer but also the survival. After diagnosis for breast
cancer, women with highest dieldrin levels survive the shortest time, on
average. A high serum dieldrin concentration was consistently related to a
subsequent poorer survival. . . . It is therefore also possible that exposure
to organochlorines somehow induces the aggressiveness of the tumor.
(Høyer et al. 2000, 323)
SEX RATIOS AFTER THE SEVESO, ITALY,

DIOXIN SPILL
The first scientific evidence that low-level dioxin pollution has a
direct effect on reproduction was revealed by Italian researchers
who studied the population of Seveso, in northern Italy, the scene
of a devastating explosion at a chemical factory in 1976 (see chapter
1). The explosion released a large quantity of dioxins into the at-
mosphere. The researchers found that babies born of women living
near the scene of the disaster had a sharply skewed sex ratio, with
more girls than boys. The effects of dioxin exposure continued to
shape the reproductive history of the area a full quarter-century
after the accident.
Paolo Mocarelli and colleagues in the department of laboratory
medicine at Desio Hospital, in Milan, found that men with the high-
Toxic Barbie? 211
est dioxin levels were least likely to father boys. The sex ratio of
children for parents aged under nineteen at the time of the accident
was 62 boys born for every 100 girls, compared with a usual sex
ratio of 106 boys to 100 girls, according to a study that was pub-
lished in the Lancet (Mocarelli et al. 2000). The families of women
who were exposed to high levels of dioxin and married men from
outside the area were unaffected. The families of exposed men who
married women from outside the area had the skewed sex ratio,
however.
This effect was evident even at very low levels of 20 nanograms
per kilogram of body weight, only twenty times the estimated aver-
age concentration of dioxin in humans in industrialized countries.
According to Mocarelli and colleagues: “The observed effects . . .
started at concentrations of less than 20 nanograms per kilogram
of bodyweight. This could have important public health implica-
tions” (1858). Specifically how dioxin affects the male reproductive
system is unclear. Scientists have reported a decreased proportion
of male births in Denmark, the Netherlands, the United States, and
Canada and in certain occupational groups, including sawmill
workers and in those exposed to air pollution from incinerators.
Professor Mocarelli said that assessing a safe level of dioxins is
complicated. “Relatively low levels of dioxin are having an effect on
males. We have shown for the first time that the human male re-
productive system is very sensitive to dioxin” (Laurance 2000). Mo-
carelli also commented, “Dioxin contamination is a world-wide
problem. These data will assist health authorities to better define
risk assessment for these toxic molecules. In fact the lowering sex
ratio in human beings has been directly linked for the first time to
male exposure to an environmental pollutant and at relatively low
doses. This effect can be tentatively interpreted as a result of dioxin
endocrine disruption of the male reproductive system” (Lancet Press
Release 2000).
SYNTHETIC ESTROGEN (DES)

Between 1945 and 1971, many women were treated with a syn-
thetic estrogen called diethylstilbestrol (DES), which was given to at
least 5 million women to prevent miscarriages and pregnancy com-
plications. The chemical was banned in 1971 after it was linked to
increases in a previously rare form of vaginal cancer. Women who
212 The Dirty Dozen
were exposed to DES in utero also have suffered an increased inci-

dence of cervical cancer in adulthood, as many of them also expe-
rienced increased fertility problems (Hines 1992). Theo Colborn and
colleagues (1993) assert that “DES-exposed humans . . . serve as a
model for exposure during early life to any estrogenic chemical”
(378).
The FDA approved DES for hormone therapy and relief of meno-
pausal disorders in 1941; during 1947, it was approved to promote
the growth of chickens and in 1949 for the prevention of miscar-
riages. The sales push for DES was undertaken despite evidence
that it was good for nothing. By 1952 at least four independent stud-
ies had reported that “women treated with DES for threatened mis-
carriages did no better than those treated with alternatives such as
bed rest or sedatives” (Colborn, Dumanoski, and Myers 1996, 54).
In 1954 DES was approved as a growth enhancer for sheep and
cattle.
By the late 1950s, DES was being promoted for a wide range of
maladies, as a miracle drug. During 1957 the Journal of Obstetrics
and Gynecology published advertising from the Grant Chemical
Company, a maker of DES, promoting it for “ALL pregnancies” to
produce “bigger and stronger babies” (Colborn, Dumanoski, and
Myers 1996, 48). Doctors prescribed DES to suppress milk produc-
tion after childbirth, to alleviate hot flashes and other symptoms of
menopause, and to cure acne, prostate cancer, and “even to stunt
the growth [of] teenage girls who were becoming unfashionably tall”
(Colborn, Dumanoski, and Myers 1996, 48).
The FDA suspended the use of DES in poultry feed in 1958 after
it was shown to be carcinogenic in experimental animals. It was
thirteen years after that, however, before its use on humans was
outlawed in 1972, the same year the U.S. EPA banned DDT. By the
time DES was banned in humans, its carcinogenic properties were
very painfully obvious.
The ban on DES use in women was provoked by Arthur Herbst,
who discovered a relationship between vaginal cancer and DES dur-
ing his tenure at Harvard Medical School and Massachusetts Gen-
eral Hospital. Commented Krimsky, “Men exposed to DES during
gestation were more likely to exhibit abnormalities in sex organs,
reduced sperm count, and lower quality of semen compared with
controls” (Krimsky 1999, 10).
In the world of toxicology, study of the DES debacle has provided
some important lessons. Experience with DES, for example, dem-
Toxic Barbie? 213
onstrated that synthetic chemicals could cross the placenta and

disrupt the extremely delicate balance of hormonal development.
The DES experience also illustrated that such contamination could
manifest itself many years after the initial shock of exposure in the
womb.
Further investigation of the effects of DES revealed that in utero
exposure resulted in a much greater incidence of cryptorchidism
and hypospadias in boys. In addition, when they reached adult-
hood, many of the same men had reduced sperm counts. The same
outcome was achieved in the male offspring of mice and rats to
which DES had been administered (Sharpe 1993). The number of
people exposed to DES (mothers and offspring) between 1950 and
1971 has been estimated at 5 to 10 million (Schettler et al. 1999,
153).
My sister, Linda Carol Edgar, was one of them. I was born January
30, 1950, six weeks early, and severely underweight, barely surviv-
ing. When my mother became pregnant with my sister Linda, she
took DES to prevent another premature birth. Nineteen months af-
ter my birth, Linda came into the world at weight and on time, as
promised. Twenty years later, she lost an ovary to that previously
rare form of cervical cancer that had suddenly become so pervasive
among women born to mothers who had taken DES to facilitate
pregnancy.
HORMONE MIMICS AND PROSTATE PROBLEMS

Prenatal exposure to hormone-mimicking substances also “may
be exacerbating the most common problem afflicting aging males:
painfully enlarged prostate glands that make urination difficult and
often require surgery” (Colborn, Dumanoski, and Myers 1996, 179–
80). Prostate cancer rates rose 126 percent in the United States
between 1973 and 1991, according to the National Cancer Institute.
Low doses of estrogen over a long period of time have been found
(by Shuk Meri Ho of Tufts University) to induce prostate cancer in
mice.
ALKYLPHENOLS AND PHTHALATES

Alkylphenols and phthalates are weakly estrogenic and have been
linked to decreased testicular size, reduced sperm counts, and male
214 The Dirty Dozen
feminization in some animal studies (Schettler et al. 1999, 179).

About 1 billion pounds of these compounds are produced in the
United States each year. They are industrial chemicals that are
widely used in detergents, paints, pesticides, plastics (including
food wraps), and many other consumer products. Alkylphenols may
be found in drinking water and leaching from plastics used in food
processing and wrapping, as well as construction materials and
children’s teething rings.
Two dozen varieties of phthalates are among the most abundant
of manufactured chemicals; they also are used in construction, in
automotive and medical industries, and in a wide variety of con-
sumer items, including many toys (the ubiquitous Barbie doll
among them), some clothing, and packaging. Most plastic wraps,
beverage containers, and linings of metal cans contain phthalates.
The most common use of phthalates is to plasticize (impart softness)
to polyvinyl chloride (PVC). Phthalates are sometimes mildly estro-
genic and have been identified as testicular and ovarian toxicants
in animal studies (Schettler et al. 1999, 181).
“Recent laboratory research in animals has linked phthalates to
damage to the liver, kidney, and testicles, as well as to miscarriage,
birth defects, and reduced fertility,” according to one researcher
(McGinn 2000, 34). Incineration of phthalates produces dioxins
also.
CONCERNS ABOUT PVC PLASTICS

During the 1990s, the market for PVCs was the fastest-growing
chlorine-related market in the world. Products manufactured from
PVCs had been incorporated into a wide variety of industrial pro-
cesses and products that most people use in their everyday lives,
from toothpaste tubes to children’s toys. If a plastic is flexible, it
probably contains PVC.
Dioxins are produced throughout the lifecycle of PVC plastic
(Thornton 1997). The manufacture of PVC begins when chlorine gas
is produced by the electrolysis of brine, during which dioxin is
formed. Chlorine is then combined with ethylene to produce ethyl-
ene dichloride (EDC). During this process large quantities of dioxins
are formed, some of which are released into the air and water. Nearly
40 percent of all the chlorine produced by the chemical industry is
used in the manufacture of PVC (Thornton 1997). Although no di-
Toxic Barbie? 215
rect comparative data exists, PVC production is probably the single

largest source of dioxins in the environment.
Joe Thornton has written, under the aegis of Greenpeace, that
“Samples taken downstream from EDC manufacturers in the U.S.
and Europe indicate significant contamination of sediment and the
food chain in the vicinity of these plants” (Thornton 1997). Green-
peace analyses at U.S. chemical facilities have indicated that wastes
from the creation of EDC are among the most intensely dioxinated
wastes anywhere. These chlorine-rich wastes often are incinerated,
producing and releasing dioxins. Once it has been created, EDC is
then converted into vinyl chloride monomer (VCM), which is poly-
merized, formulated, and formed into a final PVC-containing
product.
Plastics containing PVC thus create dioxins as they are created.
These plastics also create dioxins when they are incinerated. Di-
oxins also may be produced in other ways. When buildings or ve-
hicles are consumed by fire, dioxins usually are produced. More
typically, PVC plastics are incinerated or smelted in heat-reactive
processes that add to the ecosphere’s load of dioxins. More than 1
billion pounds of PVCs may be burned in U.S. trash and medical-
waste incinerators and in accidental structural fires each year
(Thornton 1997). Thornton adds that “The unknown quantities of
PVC burned in industrial and warehouse fires, automobile fires,
metals smelters, and wood combustion add to this total” (Thornton
1997).
Furthermore, according to Thornton, while production of many
chlorinated compounds is declining and some are holding steady,
worldwide production of PVC and its feedstocks “is rapidly growing,
both for use in the U.S. and for export, primarily to developing na-
tions” (Thornton 1997).
PVC plastic was first marketed in 1936. A 1966 Goodrich Cor-
poration memo admitted that “there is no question but that skin
lesions, absorption of bone of the terminal joints of the hands and
circulatory changes can occur in workers associated with the po-
lymerization of PVC” (Kurtz 2001, C1). “In other words, they knew
vinyl chloride could cause the bones in the hands of their workers
to dissolve,” Bill Moyers told a Public Broadcasting System audience
in March 2001 (Kurtz 2001, C1). Another document, a 1973 Ethyl
Corporation memo, says that the results of rat tests “certainly in-
dicate a positive carcinogenic effect” (Kurtz 2001, C1).
216 The Dirty Dozen
During the early 1970s, an Italian scientist, P. L. Viola (1971,

516), exposed laboratory rats to vinyl chloride and diagnosed un-
usually high rates of cancer. As Viola lowered exposure levels in his
tests, cancer persisted. A year later, another Italian researcher, Ces-
are Maltoni, found evidence of a rare liver cancer, angiosarcoma
(Moyers 2001). In Maltoni’s studies, cancer appeared in rats ex-
posed to levels of vinyl chloride that were common on factory floors
in the United States at the time. According to the report by Bill
Moyers (2001), a Union Carbide executive reported to corporate
headquarters that if a letter admitting knowledge of Maltoni’s work
ever became public, it could “be construed as evidence of an illegal
conspiracy by industry . . . if the information were not made public
or at least made available to the government.”
During the 1970s, facing mounting evidence of PVC’s toxicity, the
U.S. federal government, rejecting contrary advice from the indus-
try, ordered workplace exposure to vinyl chloride reduced to 1 ppm.
During 1974 B.F. Goodrich announced that four workers at its
Louisville, Kentucky, vinyl chloride plant had died from angiosar-
coma, a previously rare liver cancer linked to PVC manufacture, as
Maltoni had found in his study of rats. After the four deaths, 270
employees at the plant were tested. Blood abnormalities were de-
tected in 55 of them.
Moyers (2001) interviewed the wife of Dan Ross, a worker for
Conoco, and she described how he returned home one day from the
PVC plant. He took off his boots, and his wife looked at his feet. She
recalled
The whole top of ’em were burned. Now, he had on safety boots, steel-toed,
and the whole top of his feet were red where the chemicals had gone through
his boots, through his socks, under his feet, and burned them, both feet.
Later, cancer was discovered in Ross’s brain. Ross’s wife recalled

how he coped with his rapid physical decline:
You start watching him die one piece at a time, you know. It’s like, okay,
he’s blind today, but he can still hear, he can still swallow if I put something
in his mouth. But he lost the use of one of his arms, and then next day it
would be the other arm, the next day it would be one leg. And then he
couldn’t hear anymore. The hardest part was when he couldn’t speak any-
more. (Moyers 2001)
On October 9, 1990, twenty-three years to the day after he had

started working at Conoco, Dan Ross died, at age forty-six. “In the
Toxic Barbie? 217
last words he was able to speak, Dan Ross told his wife, “‘Mama,
they killed me’” (Moyers 2001).
The rising volume of PVC production is also adding to the envi-
ronment’s overload of PCB pollution. While the direct production of
PCBs was banned by the United States during 1977, this persistent
pollutant is still released into the ecosphere through the generation
of wastes, one of which is the manufacture of PVCs. In 1990 Dow
Chemical analyzed some of its chlorinated wastes and found that
they contained 302 ppm PCBs.
Manufacture of vinyl chloride monomer has caused extensive
dioxin contamination of Rotterdam harbor in the Netherlands. In
Venice, Greenpeace analyzed sediment from the Porto Marghera
that showed dioxin contamination of the lagoon by the Enichem
plant, where vinyl chloride monomer is manufactured. In Germany,
the Environmental Ministry of Lower Saxony found extremely high
levels of dioxins in sludges from the wastewater treatment plant at
Wilhelmshaven. Dioxins also were found in a dump where these
sludges were disposed (Costner 1997).
PVC-coated wallpaper and wood (often as furniture) often are
burned by individuals in their backyards, or by small companies in
inadequate furnaces that are not suited for burning such hazard-
ous wastes. In addition, in many parts of the world, plastic cable
scrap containing PVC is burned in the open air. For example, in
1994 Greenpeace discovered that imported PVC cables are recycled
in the slums of Jakarta, Indonesia, simply by burning the PVC off
the cables in big steel drums in people’s backyards (Costner 1997).
MORE POTENTIAL PROBLEMS WITH

PHTHALATES
Hair sprays, perfumes, and other brand-name cosmetics contain
toxic chemical phthalates that may be absorbed into the human
body, according to the first independent tests for these chemicals
in over-the-counter products. According to a report by Cat Lazaroff
for the Environment News Service, “Christian Dior’s Poison per-
fume, Arrid Extra Extra Dry deodorant and Aqua Net hair spray are
among many of the beauty and personal-care products that contain
one or more of the dangerous chemicals known as phthalates.” La-
zaroff’s report was drawn from a report titled Not Too Pretty, re-
leased July 10, 2002, by the Environmental Working Group,
218 The Dirty Dozen
Coming Clean, and Health Care without Harm. The groups con-
tracted with a major national laboratory to test seventy-two name-
brand, off-the-shelf beauty products for the presence of phthalates,
a large family of industrial chemicals linked to birth defects in the
male reproductive system. The lab found phthalates in fifty-two of
the seventy-two, or 72 percent, of the products tested. Only one of
the products listed phthalates on the label (Lazaroff 2002).
Phthalates are used as a plastic softener and solvent in several
consumer products. In cosmetics and other beauty products,
phthalates help make nail polish chip-resistant and extend the life
of perfumes’ fragrance. According to this report, these chemicals
can be absorbed through the skin, inhaled as fumes, ingested when
they contaminate food or when children bite or suck on toys, and
inadvertently administered to patients from plastic medical devices
containing PVC. Numerous animal studies have demonstrated that
phthalates can damage the liver, kidneys, lungs and reproductive
system, particularly the developing testes, the groups sponsoring
the study asserted (Lazaroff 2002).
According to the Environment News Service report, One Centers
for Disease Control (C.D.C.) study found that 5 per cent of women
of reproductive age—an estimated two million women—may be get-
ting up to 20 times more of the phthalate D.B.P. than the average
person in the population. The highest exposures for women of child-
bearing age were above the federal safety standard, which may cre-
ate a risk of reproductive birth defects, based on animal studies
considered relevant to humans (Lazaroff 2002).
In reply, the Cosmetic, Toiletry and Fragrance Association (CTFA),
an industry group, said that the use of phthalates in cosmetics and
personal care products is supported by “an extensive body of sci-
entific research and data that confirms safety. The Food and Drug
Administration (F.D.A.), the Environmental Protection Agency
(E.P.A.), Health Canada and other scientific bodies. In Europe,
North America, and Japan have examined phthalates and allow
their continued use,” the CTFA said (Lazaroff 2002). “Phthalates
were also reviewed by the Cosmetic Ingredient Review (C.I.R.), an
independent body that reviews the safety of ingredients used in cos-
metics,” the group added. “C.I.R. found them to be safe for use in
cosmetics in 1985” (Lazaroff 2002). The CIR’s expert panel voted
to begin a re-review of phthalates. The CTFA acknowledged but
stressed that the re-review “does not suggest that a previous con-
Toxic Barbie? 219
clusion will be changed, only that there is sufficient new informa-

tion that should be evaluated” (Lazaroff 2002).
“The testing done for Not Too Pretty covers less than one per cent
of the beauty products sold in drug and discount stores across the
United States, but it appears to be the most comprehensive testing
ever made available to American consumers,” said Charlotte Brody,
executive director of Health Care without Harm. “Because of lax
F.D.A. labeling rules, we cannot know how many more beauty prod-
ucts contain unlabeled quantities of phthalates” (Lazaroff 2002).
According to the Environment News Service, the limited testing
done for Not Too Pretty revealed that the same companies that pro-
duce phthalate-laden beauty products also make products free of
phthalates. For example, Unilever makes hair sprays with phthal-
ates—Aqua Net and Salon Selectives—and without phthalates—
Thermasilk and Suave. L’Oreal markets Jet Set nail polish without
DBP but puts the phthalate in its Maybelline brand. Procter and
Gamble sells Secret Sheer Dry deodorant with phthalates and Se-
cret Platinum Protection Ambition Scent without phthalates. Louis
Vuitton has taken phthalates out of its Urban Decay nail polish but
still has these chemicals in Christian Dior nail polish and the fra-
grance Poison (Lazaroff 2002).
Samuel S. Epstein, chairman of the Cancer Prevention Coalition,
and professor emeritus, Environmental Medicine, University of Il-
linois School of Public Health, Chicago, wrote in a commentary for
the Environment News Service, “With rare exceptions such as chil-
dren’s bubble baths, the Food and Drug Administration has never
required the industry to label its products with any warning of well-
documented risks, particularly reproductive and cancer; nor has
the F.D.A. banned the sale of unsafe products to an unsuspecting
public, although so explicitly authorized by the 1938 Food, Drug
and Cosmetics Act” (Epstein 2002).
The Environmental Health Network of California during mid-2002
petitioned the U.S. Food and Drug Administration asking for warn-
ing labels on cosmetics to identify allergens and hazardous sub-
stances contained in the hair spray, deodorant, nail polish, and
perfume. Epstein said that the labels are especially important for
phthalates in perfumes and fragrances, to which about 12 percent
of the population are sensitive (“Labeling Cosmetics” 2002).
The fragrance industry uses phthalates to make scents evaporate
more slowly; “Phthalates in fragrances make the scent last longer,”
220 The Dirty Dozen
the American Chemistry Council wrote July 10 in “Phthalates and

Your Health” (“Labeling Cosmetics” 2002). Besides some twenty
allergens, cosmetics and toiletries contain other numerous hazard-
ous ingredients, says Epstein. “These include about 100 carcino-
gens and 15 endocrine hormonal disrupters” (“Labeling Cosmetics”
2002). As a variety of products is used by a single person, compli-
cating factors come into play that Epstein calls “hidden” carcino-
gens. “These include those contaminating non-carcinogenic
ingredients, those formed in the product or skin by the breakdown
of non-carcinogenic ingredients, and those formed by the chemical
interaction between ingredients or contaminants,” he says (“Label-
ing Cosmetics” 2002).
EUROPEAN PARLIAMENT VOTES TO

ELIMINATE PVCS
Concern regarding estrogenic properties of PVCs reached a level
in Europe that provoked, on April 3, 2001, a European Parliament
vote to eliminate polyvinyl chloride plastics. “The European Parlia-
ment has recognized the dangers associated with PVC production,
use and disposal and voted in the interests of the environment and
public health. This is an important step towards effective action
against the many hazards of PVC plastic and the need to use safer
materials. Evidence that PVC harms the environment and human
health is overwhelming and, as today’s vote reflects, there is now
only one way forward: PVC has got to go,” said Greenpeace cam-
paigner Maureen Penjueli (“European Parliament” 2001).
The European Parliament voted in favor of introducing a substi-
tution policy, starting with replacement of soft PVC. The same Eu-
ropean union vote also called for a ban of lead additives in PVC and
for compulsory marking of PVC products, as well as separate col-
lection of PVC waste. Moreover, the parliament said that incinera-
tion and landfills are unsustainable options for PVC disposal.
Combustion of PVC leads to hazardous emissions in the atmo-
sphere, such as dioxin, and produces toxic ash that has to be
landfilled.
“Concern over the hazards of PVC plastic is widespread. Local
communities, health groups, consumer groups and industry have
all been calling on the E.U. to phase out this dangerous plastic,”
said Penjueli. “It’s heartening that finally their concerns have been
validated and their voices heard. It is now vital that the European
Toxic Barbie? 221
Commission proposes a directive to act on today’s decisions,” she

added.
TOXIC BARBIE?
Information presented during late August 2000 at an American
Chemical Society meeting in Washington, D.C., suggested that
some vintage toys (including older Barbie dolls) may ooze PVC as
they age, exposing children to endocrine-disrupting chemicals.
Yvonne Shashoua, a conservation scientist and chemist with the
National Museum of Denmark in Copenhagen, told the meeting that
some old Barbie dolls manufactured in the early years after the
plastic princess’s first release in 1959 contain PVC (Schwanke and
Yoder 2000).
Deteriorating Barbie dolls may become sticky, with heat and sun-
light accelerating the process. Shashoua says that use of the trou-
blesome substance has been generally banned, and a new formula
now used in PVC products does not pose a known health risk. (That
is to say, no health risk for which the replacement substances have
been tested, which is not a guarantee of safety, given the way re-
search follows use of many chemicals.)
ESTROGEN MIMICRY AND HEATED PLASTIC

Even microwaved plastic may mimic estrogen. David Feldman of
the Stanford University Medical School, who, with colleagues, was
seeking the evolutionary origins of steroids (the hormone) found un-
explained estrogen mimics in their laboratory samples. They tried
and failed to purge the substances from their equipment, even in
otherwise sterile samples. Feldman and colleagues learned even-
tually that estrogen mimics were leaching from the polycarbonate
flasks used to sterilize water for experiments, as they detected bis-
phenol A, a synthetic estrogen, leaching from their plastic lab
equipment.
Bisphenol A is similar in molecular structure to DES and also acts
estrogenically, but with one-thousandth or two-thousandths the
potency. Leaching generally takes place when the plastic is heated.
Some plastics (usually those that are more rigid to the touch) do not
leach when heated, but softer ones do. If the plastic interacts with
the food when it is heated, it may be leaching synthetic estrogens.
222 The Dirty Dozen
This is the same problem as with old Barbie dolls made of PVC,
which does leach estrogen mimics when it is heated (Feldman et al.
1984).
Bisphenol A also has been detected in the plastic linings inside
many metal food cans (the plastic lining is meant to keep the food
from mixing with residues from the metal). Nicholas Olea found that
many of these cans with epoxy-based linings “contained Bisphenol
A in sufficient quantities that they could make breast cancer cells
divide” (Cadbury 1997, 150; Brotons et al. 1995). While natural es-
trogens are eliminated from the body by natural processes, the syn-
thetics “have the ability to remain in the body for months or years,
building up a reservoir in the fat stores” (Cadbury 1997, 171).
RESEARCH NEEDED ON ESTROGEN MIMICS

In August 2000 the National Research Council of the U.S. Na-
tional Academy of Sciences made public its long-awaited report,
Hormonally Active Agents in the Environment. The report cited much
of the research by Theo Colborn and others and stressed that hor-
mone disruption is a serious scientific issue deserving of funded
research. The potential of endocrine disruption was one of the major
elements compelling representatives from about one hundred
twenty countries to finalize a ban, in Stockholm, of the dirty dozen
organochlorines in December 2000. The detected range of effects
keeps expanding, over time, as the amount of any given chemical
thought to pose a threat keeps dropping.
A National Toxicology Program coordinated by the National Insti-
tute of Environmental Health Sciences issued a report that brought
back something of a hung jury on the question of low-dosage endo-
crine disrupters: “Several studies provide credible evidence for low-
dose effects of bisphenol A; these include increased prostate weight
in male mice at six months of age” (National Toxicology Program
2000, iii). However, other studies using other rats in other settings
found no evidence. The panel concluded that while there is “credible
evidence that low doses of BPA [bisphenol A] can cause effects on
specific endpoints. . . . [but] the panel is not persuaded that a low-
dose effect of BPA has been conclusively established as a general or
reproducible finding” (National Toxicology Program 2000, iv; see
also vom Saal et al. 1997). The same report found that low-dose
effects “were clearly demonstrated for estradiol and several other
estrogenic compounds” (National Toxicology Program 2000, iv).
Toxic Barbie? 223
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8
Solutions: Public Policy Issues
THE STOCKHOLM CONVENTION ON

PERSISTENT ORGANIC POLLUTANTS: AN
INTERNATIONAL BAN ON POPS
While world diplomacy has thus far proved inadequate to the
challenges of global warming, POPs have been rather quickly
banned by an international agreement that is being ratified as this
book is being written. Evidence of health damage from POPs (es-
pecially among the Inuit and animals of the Arctic) is so easily rec-
ognizable that even the George W. Bush White House quickly
announced support for the Stockholm Convention to eliminate
POPs. Such support does not begin the endgame for the Stockholm
Convention, however. During the next several years, meeting the
goals of the convention will require basic changes in the manufac-
turing processes of many products that are used by many millions
of people worldwide. The Stockholm Convention eventually will re-
quire entire industries to find new ways to produce even basic com-
modities such as steel and to dispose of waste without emitting the
newly banned by-products.
The Stockholm Convention requires that nine of the dirty dozen
be removed completely from use and production: aldrin, chlordane,
toxaphene, dieldrin, endrin, heptachlor, hexachlorobenzene, mirex,
and toxaphene. Exceptions to complete elimination have been al-
lowed for dioxins and furans, which are to be reduced immediately
and eventually eliminated “where feasible,” by restrictions on open
trash burning, for example (Kaiser and Enserink 2000, 2053).
The Stockholm Convention provides an exemption for DDT when
it is used to control malaria. Malaria killed 2.7 million people world-
230 The Dirty Dozen
wide in 1999; it is the world’s single deadliest disease, claiming more

lives than AIDS/HIV, and its toll is growing. Malaria experts testified
at the Stockholm negotiations that no feasible substitute exists for
malaria control, DDT’s original use during World War II. About
twenty-five countries still find DDT necessary for use against ma-
laria. The Stockholm Convention urges intensified research into
identifying alternatives to DDT. Countries using DDT are required
to document who is utilizing it, and under what circumstances, in
a special register.
Even with a world protocol that aims to eliminate them, the dirty
dozen (and many other organochlorines) will be with us as serious
environmental pollutants for several decades to come at least. Not
only are they long-lasting in the atmosphere, but industries that
produce them have become expert at semi-green shuck and jive that
announces compliance while ducking speedy implementation of
new rules.
Representatives from about one hundred twenty countries agreed
on the Stockholm Convention during December 2000. Five months
later, on the eve of Earth Day 2001, U.S. President George W. Bush
agreed to sign the Stockholm Convention on Persistent Organic Pol-
lutants and said he would submit it to the U.S. Senate for ratifica-
tion. Coming within a month of Bush’s repudiation of the Kyoto
Protocol (meant to reduce emissions of greenhouse gases), the
Stockholm Convention has some diplomatic virtues from the stand-
point of U.S. interests. First, the United States, which already had
banned many of the dirty dozen, has little to lose, in contrast with
any meaningful effort to reduce global warming. The production of
carbon dioxide and methane (the two main greenhouse gases) are
intricately wedded to our fossil-fueled industrial base.
The Stockholm Convention was the result of nearly two decades
of international diplomacy aimed at restricting and eventually end-
ing the manufacture and use of the most notorious POPs. With their
threat to stratospheric ozone becoming more evident during the
1980s, CFCs were the first major organochlorine to be restricted by
the Montreal Protocol in 1987.
At the 1992 Earth Summit in Rio de Janeiro, more than one hun-
dred seventy governments committed in their Agenda 21 to elimi-
nate emissions of organohalogen and other synthetic compounds
that threatened to accumulate to dangerous levels. The UN Envi-
ronment Program’s (UNEP) May 1995 Governing Council agreed to
Solutions 231
initiate an expedited assessment of the twelve priority POPs and

their alternatives. In June 1995 the governments of Canada and the
Philippines held an international experts’ meeting on POPs in Van-
couver. The final consensus statement of that meeting stated that
“There is enough scientific information on the adverse human
health and environmental impacts of POPs to warrant coherent
action at the national, regional, and international level. This will
include bans, phase-outs and provisional severe restrictions for cer-
tain POPs” (World Wildlife Fund 2000).
With this scientific consensus in hand, a global UNEP conference
convened in November 1995 in Washington, D.C. Although its focus
was on protection of the marine environment from land-based ac-
tivities, special attention was devoted to POPs, with a high-level
ministerial segment agreeing by consensus that “International ac-
tion is needed to develop a global, legally binding instrument,
amongst other international and regional actions, for the reduction
and/or elimination of emissions and discharges, whether inten-
tional or not, and where appropriate, the elimination of the manu-
facture and use of [the twelve priority POPs]” (World Wildlife Fund
2000).
The Intergovernmental Forum on Chemical Safety (IFCS) devel-
oped recommendations (Buccini 1996) in 1996 that concluded that
sufficient evidence existed to warrant a global treaty to minimize
the risk from the twelve specified POPs. IFCS called for immediate
action by UNEP and the World Health Assembly to reduce or elim-
inate POPs emissions and discharges. In February 1997 the UNEP
Governing Council endorsed IFCS’s recommendations and agreed
by consensus to move forward with treaty negotiations.
During these early negotiations on an international ban of POPs,
officials from the World Health Organization (WHO) and delegates
from several developing countries questioned the elimination of
DDT because of its major role in combating malaria and other
insect-borne diseases. Malaria poses a threat to at least 2.5 billion
people in more than ninety countries and contributes every year to
about three million deaths, over half of them children under five
years old. Although the WHO and its experts have slowly embraced
disease-fighting methods that reduce the reliance on DDT, African
delegates stress the need to find and fund cost-effective alter-
natives.
Negotiators also faced the question of how to identify, collect, and
destroy POPs that remain in obsolete stockpiles of persistent chem-
232 The Dirty Dozen
icals or in hot spots of environmental contamination. In a number

of developing countries, obsolete pesticides, including POPs, are
stored in extremely hazardous conditions, as are old PCB-
containing transformers and capacitors.
The Stockholm Convention seeks, within some practical limita-
tions, to realize a point of view enunciated by the World Wildlife
Fund:
Our decades of experience with persistent chemicals have demonstrated
unequivocally that there is no way to manage POPs. The only responsible
course is to eliminate their production, use, and release as quickly as pos-
sible, while recognizing and addressing the special circumstances of devel-
oping countries in need of assistance. The time has come to stop this
experiment with “hand-me-down poisons” before it does more irreparable
damage to wildlife, children, and adults. (World Wildlife Fund 2000)
The Stockholm Convention on Persistent Organic Pollutants will

be legally binding once 50 of the 122 signatory nations have ratified
it, a process that could take several years. The new protocol also
contains mechanisms for adding other chemicals to be banned in
future years.
The Stockholm Convention requires rich nations to pay develop-
ing countries to phase out the banned pollutants and to destroy
stockpiles, mostly within five years of ratification. Use of these pol-
lutants after that time will require stringent proof of need. In the
case of PCBs, which have been widely used in electrical transform-
ers and other equipment, governments may maintain existing
equipment in a way that prevents leaks until 2025 to allow time to
arrange for PCB-free replacements. Although PCBs are no longer
produced, hundreds of thousands of tons are still used in such
equipment. In addition, a number of country-specific and time-
limited exemptions have been established for other chemicals. The
Stockholm Convention also includes plans for a $150 million fund
to be managed by the United Nations that will help Third World
countries dispose of toxic stockpiles of gift waste (see chapter 4).
Experts opened talks in mid-January 2002 in Geneva to develop
policies and technical guidelines for a major treaty on transporting
and discarding toxic pollutants under the Stockholm Convention
banning POPs and other programs under the aegis of the United
Nations. The convention’s Technical Working Group developed
technical guidelines for environmentally sound management of
waste lead-acid batteries, metal and metal compounds, plastic
Solutions 233
wastes, and POPs and the dismantling of ships. These issues are
covered by the Basel Convention on the Control of the Trans-
boundary Movements of Hazardous Wastes and Their Disposal.
The Basel Convention was adopted in March 1989 after a series
of notorious toxic cargoes from industrialized countries drew public
attention to the dumping of hazardous wastes in developing and
East European countries. The treaty, which has 149 parties, obliges
its members to ensure that such wastes are managed and disposed
of in an environmentally sound manner. Governments are expected
to minimize the quantities that are transported, to treat and dispose
of wastes as close as possible to where they were generated, and to
minimize the generation of hazardous waste (“Hazardous Waste
Treaty” 2002).
The day before these discussions began, Turkish police arrested
seventeen Greenpeace activists who had occupied a Swiss ship at a
ship-breaking yard in Aliaga, Turkey. Unfurling a banner that said
“Stop Toxic Shipbreaking” from on board the Star of Venice, the
Greenpeace representatives demanded an end to the practice of
scrapping ships that contain toxic materials on Turkish beaches.
Even as international diplomacy works out an eventual ban of
them, release of POPs into the environment is continuing, and a
possibility exists for further severe impacts on the health of wildlife
and humans. Of particular concern are effects on the developing
stages of life, the unborn and nursing young. Furthermore, in ad-
dition to POPs targeted by international diplomacy, there are many
other POPs and hazardous chemicals that are toxic to health. Many
POPs remain in the atmosphere (notably in the Arctic and Antarctic)
for a century or more, and so the struggle to restore the ecosystem
will be long and difficult.
In mid-April 2002 the Bush administration submitted the Stock-
holm Convention on Persistent Organic Pollutants to the U.S. Sen-
ate for ratification. Additional legislation to amend existing U.S.
laws needed to implement the POPs treaty and two related treaties
also was directed to Congress at the same time. The Bush legislation
restricts the treaty in one important way, however: it lacks provi-
sions contained in the Stockholm Convention to add other chemi-
cals to the banned list in the future. “The Bush administration
proposal ties the Environmental Protection Agency’s hands, limiting
domestic implementation to 12 POPs already regulated in the U.S.,”
said public health expert Robert Musil, who is chief executive officer
and executive director of Physicians for Social Responsibility. “Con-
234 The Dirty Dozen
gress must now come forward with legislation that will implement
the full intent of the POPs treaty as a dynamic, flexible instrument
to protect human health now and into the future,” he urged (“POPs
Treaty” 2002).
PROBLEMS WITH “PROOF”

The Stockholm Convention was negotiated despite arguments on
some fronts that participants lacked absolute scientifically valid
proof that the dirty dozen are environmentally harmful. The Wey-
bridge Report outlines some of the problems with such a standard
of proof:
It is not possible fully to understand the significance of levels found in tis-

sues or blood until the mechanism and timing of action of EDS [endocrine
disrupting substances] and their metabolites are better understood. . . . It
is not anticipated that any useful SAR [structure-activity relationships] . . .
will emerge.” (European Workshop 1997, 1: 37, 45)
The same report also stresses (1: 41) that “potential interactive ef-
fects of exposure to several substances simultaneously need to be
taken into account.”
The structures of endocrine-disrupting chemicals vary widely,
and so, according to Peter Montague, “No structure-activity rela-
tionships are likely to emerge to help scientists decide which ones
are bad actors. This means all chemicals are candidates for testing,
which greatly complicates (and boosts the price of) testing to find
endocrine disrupters” (Montague 1997). Test-tube examination of
chemicals will not yield the needed information, according to Mon-
tague, who has written that tests must be done on living animals
that are expensive and often cruel (Montague 1997).
The necessary tests for the thousand most common toxic chem-
icals in unique combinations of three “would require at least 166
million different experiments,” according to Montague (1997). This
means that endocrine disrupters could have substantial effects that
will demonstrate acceptable proof under laboratory standards.
Montague described the absurdity of the situation:
If we wanted to conduct the 166 million experiments in just 20 years, we

would have to complete 8.3 million tests each year. The U.S. presently has
the capacity to conduct only a few hundred such tests each year. Just train-
Solutions 235
ing sufficient personnel to conduct 8.3 million animal tests each year is
beyond our national capacity. (Montague 1997)
Because verifiable scientific proof is so elusive, the Weybridge Re-

port recommends use of the Precautionary Principle (1: 52). Devel-
oped at the Rio Earth Summit (1992), the Precautionary Principle
holds that “Where there are threats of serious or irreversible dam-
age, lack of full scientific certainty shall not be used as a reason for
postponing cost-effective measures to prevent environmental deg-
radation” (Bodansky 1994, 203). The chemical industry has long
argued that harm should be proven before products are removed,
but environmentalists believe the search for a largely unachievable
degree of scientific certainty is a corporate stalling tactic.
REQUIRE COMPLICIT COMPANIES TO PAY

FOR CLEANUP
During 2002, companies found responsible for PCB contamina-
tion in Anniston, Alabama, were required to pay costs associated
with its cleanup. In late March the U.S. Justice Department and the
U.S. EPA reached an agreement with Solutia, Incorporated (for-
merly Monsanto Company) and Pharmacia Corporation to clean up
PCBs that leaked from a former Monsanto plant in western Annis-
ton. The PCBs continued to contaminate air and water of several
low-income neighborhoods, regional waterways, and about forty
miles of floodplain in the area. The corporate-funded cleanup was
in lieu of a Superfund listing for the community, requiring tax-
assisted cleanup. According to an account by the Environment
News Service, Solutia and Pharmacia agreed to emergency cleanup
of the worst residential contamination in the area.
Under the pact, according to ENS, Solutia and Pharmacia were
required hire EPA-approved contractors to study all contaminated
areas for PCBs and other environmental pollutants, and evaluate
the risk they pose to public health and the environment. The study
will determine available cleanup options and suggest a strategy for
restoring the community, covering all areas where PCBs have been
found, including the Solutia facility, the landfills, creeks, rivers,
lakes, flood plains and residential, commercial and agricultural
properties that surround the facility (“Settlement” 2002). The agree-
ment also includes establishment of a $3.2 million foundation for
special-education needs of children in the Anniston area. The com-
236 The Dirty Dozen
panies also were required to pay the EPA as much as $6 million for
the agency’s investigative costs.
Some community activists (such as members of the Anniston-
based Community against Pollution) feared, however, that the com-
plicit companies may be using the agreement as a stalling tactic.
Their fears were supported when Solutia filed a petition in court
asking that a lawsuit seeking a court-ordered cleanup be dismissed.
SEEKING A BAN OF PVCS

At the top of many environmental activists’ lists of POP-related
business is a ban of PVC production. Greenpeace recommends a
phase-out of PVC production and use, and the European Union has
taken a major step toward that goal (see chapter 7). As Joe Thornton
has written:
The health risk posed by dioxins calls for immediate action to reduce and
ultimately eliminate the production and use of PVC. PVC is the single largest
use of elemental chlorine and its production is expanding. It is also known
that dioxin is generated as a byproduct during PVC production, use, or
treatment for disposal. There are strong grounds for holding PVC respon-
sible for a substantial and growing proportion of global dioxin production
and release. . . . Reducing the production and use of PVC is a simple and
effective avenue to prevent PVC-related dioxin pollution. By replacing PVC
with alternative, chlorine-free materials, dioxin formation associated with
PVC can be eliminated entirely. Given the importance of the PVC lifecycle
in the nation’s dioxin burden, a PVC phase-out must be a top priority in
any dioxin-prevention strategy. (Thornton 1997)
According to another observer, “The single most effective way to

lower dioxin output is to get as much chlorine as possible out of the
waste stream. PVC is the source of an estimated 80 percent of the
chlorine that flows into municipal waste incinerators and nearly all
the chlorine in medical waste incinerators” (McGinn 2000, 36).
Numerous businesses have eliminated or begun working toward
a PVC phase-out in their products and facilities, including Nike,
Volvo, Saab, Braun, Ikea, the Body Shop, and Svenska Bostder (one
of Sweden’s leading construction companies). Major construction
projects such as the Sydney 2000 Olympic village were designed to
minimize the use of PVCs “by selecting alternative materials where
they are available, are fit for the purpose and are cost-competitive”
(David Richmond, director general of the Sydney 2000 Olympic Co-
Solutions 237
ordination Authority, to Nicole Williams, chief executive of the Plas-

tics and Chemicals Industries Association, May 15, 1998, cited in
Cray and Hardin 1998).
CHANGE THE EPA’S REVIEW PROCEDURES

Scientists and other experts who advise the EPA on regulations
governing toxic chemicals sometimes maintain ties with the affected
industries (among other conflicts of interest), according to a study
by the General Accounting Office (GAO). Congress established EPA
science advisory boards in 1978 to provide independent analysis via
peer review in a balanced manner. The report asserted that the EPA
had failed to probe adequately for panel members’ ties to the chem-
ical industry.
According to the Washington Post, “The report found serious de-
ficiencies in the EPA’s procedures for preventing conflicts of interest
and ensuring a proper balance of views among members of Science
Advisory Board panels. For example, four of the 13 panel members
who studied the cancer risks of the toxic chemical 1,3-butadiene in
1998 had worked for chemical companies or industry-affiliated re-
search organizations—including one who had worked for a com-
pany that manufactured 1,3-butadiene, according to the report”
(Pianin 2001, A-2).
The GAO identified similar problems with three other cancer-risk-
assessment panels. “In one case,” according to the Post report,
“Seven of 17 advisory-board members worked for chemical com-
panies or for industry-affiliated research organizations. Five other
panelists had received consulting or other fees from chemical man-
ufacturers” (Pianin 2001, A2). “The regulatory process benefits from
scientific and technical knowledge, expertise and competencies of
panel members,” the report stated. “However, the work of fully com-
petent peer review panels can be undermined by allegations of con-
flict of interest and bias” (Pianin 2001, A2). “The American people
expect decisions that affect environmental and public health regu-
lations to be based on unbiased science,” Rep. Henry A. Waxman,
Democrat of California, said, “but this GAO study reveals polluting
industries are in a position to influence panel findings” (Pianin
2001, A2).
Before the release of this report, Greenpeace and the Center for
Health, Environment, and Justice already had complained about
238 The Dirty Dozen
the composition of an EPA panel convened to study the health ef-

fects of dioxin. About one-third of the twenty-one panel members
had worked as paid consultants to the chemical industry, according
to the GAO study (Pianin 2001, A2). Erik Olson of the Natural Re-
sources Defense Council, an environmental group, said that “we’re
seeing . . . advisory board panels—stacked with industry mouth-
pieces—acting like kangaroo courts to strike down important EPA
initiatives” (Pianin 2001, A2). The panel’s composition was a major
reason that the EPA did not officially recognize the carcinogenic na-
ture of dioxins until 2000, long after the U.S. armed forces began
giving medals to veterans who suffered cancers (and other maladies)
from Agent Orange toxicity three decades earlier.
As controversy surfaced at EPA regarding possible conflicts of in-
terest on its review panels, questions were being raised during the
summer of 2001 about President George W. Bush’s nominee to head
an obscure but powerful White House agency, the Office of Infor-
mation and Regulatory Affairs, which is part of the Office of Man-
agement and the Budget. Its administrator acts as a regulatory czar
who can block any new regulation, whether arsenic standards for
drinking water, worker-protection rules, or the public’s right to
know (Durbin 2001).
As a participant in the aforementioned EPA Science Advisory
Board subcommittee on dioxin, John Graham, Bush’s nominee,
had said that reducing dioxin levels too far might “do more harm
. . . than good.” Graham also asserted that dioxin might prevent
cancer in some cases, a hypothesis that a senior EPA official called
“irresponsible and inaccurate.” Graham also told Congress that
smog protects people from the harmful effects of too much sunlight.
Graham also rejected the idea that pesticides in foods may pose
health problems, calling this a “trivial” concern that reflects public
“paranoia” about toxic chemicals (Durbin 2001, A15).
“There is no justification for completely abandoning chemicals per
se as components in the defensive toolbox for managing pests”
(Committee on the Future Role 2000, 253). “A concerted effort in
research and policy should be made to increase the competitiveness
of alternatives to chemical pesticides” (Committee on the Future
Role 2000, 255). The need for alternative methods is underscored
by the fact that “pesticide resistance now is universal across taxa”
(Committee on the Future Role 2000, 257).
Solutions 239
TAXATION
A tax has been proposed on the chlor-alkali process per ton of
chlorine produced. Revenue, under this proposal, would be held in
a fund to aid the transition to a chlorine-free industrial society. In
particular, funds should be used for exploring and demonstrating
economically viable alternatives and for easing dislocations among
affected workers and communities. In addition, funds should be
targeted toward clean production processes to assist developing
countries and small businesses in making the change (Allsopp et
al. 1995).
EATING ORGANICALLY
The organic-food market in the United States generated $178 mil-
lion in 1980, $2.8 billion in 1995, and more than $5.4 billion in
1998. There were 2,841 U.S. organic farms in 1991, 4,060 in 1994,
and 12,000 in 1997 (Committee on the Future Role 2000, 113). By
the late 1990s, organic-food sales were increasing 20 percent a year
in the United States (Committee on the Future Role 2000, 145). The
sustained increase in of the market for organic produce is undoubt-
edly a reaction, at least in part, to rising anxiety about organochlo-
rines in food.
GOING NONTOXIC: WISCONSIN’S POTATO

FARMERS
Since 1995 Wisconsin potato farmers have made a concerted ef-
fort to slash their usage of several toxic chemicals, reducing their
consumption of them by a half million pounds in three years. The
reductions were described in a report by the World Wildlife Fund,
the Wisconsin Potato and Vegetable Growers Association, and the
Integrated Pest Management team at the University of Wisconsin
(“A Report” 2000). Wisconsin potato farmers have reduced their use
of eleven high-risk pesticides.
The farmers used integrated pest-management techniques such
as scouting and spot-treating for pests, computer prediction models
to determine when pests are most active, and intensive crop rota-
tions. Some of the farmers also used newer, less toxic pesticides.
Wisconsin farmers annually plant 80,000 acres of potatoes, making
240 The Dirty Dozen
Wisconsin the third-largest potato-producing state (“A Report”

2000).
The Wisconsin farmers acted early to reduce vulnerability to regu-
lation, address the increasing problem of pesticide resistance, and
protect the quality of wildlife habitat. The Wisconsin program could
provide a model for other farmers in other states and nations.
PULP AND PAPER: GETTING THE CHLORINE

OUT
Chlorine use by paper producers has been declining significantly.
The paper-making industry once consumed one-sixth of all chlorine
produced, making it the second-largest chlorine-using industry
(PVC plastic manufacture is the largest). Pulp and paper mills that
use older chlorine-gas bleaching methods create and release highly
toxic and persistent organochlorine chemicals.
Elimination of chlorine-based bleaching by the paper industry is
well underway in Europe. Most of the twenty-eight mills worldwide
that were producing commercial quantities of chlorine-free kraft
pulp by 1994 were located in Europe. In 1993, 34 percent of all
printing paper (excluding newsprint) sold in the Germanic and
Scandinavian countries of Europe was chlorine-free. Industry
sources forecast that by 1996, this percentage will double to 68 per-
cent (Palter and Weinberg 1994). The German weekly newsmagazine
Spiegel converted to chlorine-free paper in response to growing
pressure from environmentalists. Other magazine publishers
followed.
Some book publishers have been purchasing only chlorine-free
paper. The Cornell University Press says as much on the copyright
pages of its books:
Cornell University Press strives to use environmentally responsible sup-

pliers and materials to the fullest extent possible in the publishing of its
books. Such materials include vegetable-based, low-VOC inks and acid-free
papers that are recycled, totally chlorine-free, or partially composed of non-
wood fibers. Books that bear the logo of the FSC (Forest Stewardship Coun-
cil) use papers taken from forests that have been inspected and certified as
meeting the highest standards for environmental and social responsibility.
(Huhndorf 2001, copyright page)
For several years an American Library Association task force on

the environment tried to get the ALA Council to endorse a resolution
Solutions 241
advocating use of chlorine-free papers, which may be bleached with

oxygen or hydrogen peroxide. After almost four years, this standard
was largely adopted.
As a result of bleaching process changes and strict EPA stan-
dards, releases of dioxins from the nation’s nearly one hundred
bleached-pulp mills have dropped by at least 94 percent since 1988.
Dioxins have been eliminated from the wastewaters of some mills
that have switched to largely chlorine-free technology.
BANNING BACKYARD TRASH INCINERATION

One substantial remaining uncontrolled source of dioxin release
into the environment is residential waste incineration, including
backyard burning of trash, most notably in rural areas without
garbage pickup service. Such burning is “one of the largest unad-
dressed dioxin sources and one that could have a disproportionately
large contribution to the [toxicity of the] food supply,” the U.S. EPA
has stated (Skrzycki and Warrick 2000, A1).
A PCB-EATING BACTERIUM?
Researchers have discovered a strain of bacteria capable of break-
ing down the toxic PCBs that contaminate soil and sediments near
many industrial sites. The bacterium breaks down tough chlorine
bonds in PCBs in river and harbor sediments. The discovery of the
bacterium was reported in Environmental Microbiology by scientists
with the University of Maryland Biotechnology Institute (UMBI)
(“Bacteria Breaks Down” 2002).
In experiments using bottom sediments from Baltimore Harbor,
researchers of UMBI’s Center of Marine Biotechnology (COMB) and
the Medical University of South Carolina (MUSC) discovered the
PCB-degrading bacterium using a rapid DNA screening method. Ac-
cording to a report by the Environment News Service, “Particles of
PCBs persist after many years, because they don’t dissolve well in
water. They attach to sediment and get covered over,” said Kevin
Sowers, research microbiologist at COMB. “Unless there is some
turnover, a lot of PCBs stay hidden” (“Bacteria Breaks Down” 2002).
“This first identification of a PCB dechlorinating, anaerobic [with-
out oxygen] bacterium is important for bioremediation efforts and
for developing molecular probes to monitor PCB degrading where
242 The Dirty Dozen
they are found,” said Sowers (“Bacteria Breaks Down” 2002). The
researchers linked PCB dechlorination to the growth of the bacte-
rium, which appears to live off the compound. “This is a great
example of how manmade pollution can be handled by micro-
organisms through their incredible ability to adapt,” said Jennie
Hunter-Cevera, UMBI president and environmental biotechnologist
(“Bacteria Breaks Down” 2002). The report concludes that the UMBI
method could be used to identify additional PCB-degrading
microbes.
PROSECUTING THE FRIO BANDITOS

By 2002 CFC smuggling was becoming more than a legal curi-
osity, with more cases coming to light. By the early years of the third
millennium, according to the U.S. Environmental Investigation
Agency, the Frio Banditos were serving a multimillion-dollar inter-
national market that spans the United States and several Third
World nations. Transactions had reached 20,000 tons a year
(“Smuggled C.F.C.s” 2002).
A Florida man faced a fine and possible jail time for smuggling
CFCs into the United States. Clifford Windsor of Fort Lauderdale,
pleaded guilty on December 19, 2001, to violating the Clean Air Act
by illegally importing about three hundred cylinders of Freon-12, a
CFC refrigerant, some of which were sold to businesses. The con-
viction carries a maximum sentence of up to five years in prison and
a fine of up to $250,000. The case was investigated by the U.S. EPA’s
Criminal Investigation Division, the U.S. Coast Guard, the U.S.
Customs Service, and the Ft. Lauderdale Police Department
(“Smuggled CFCs” 2002). Before the Montreal Protocol, the refrig-
erant R-12 was used legally in air conditioners in automobiles man-
ufactured before 1994.
GARDENING WITHOUT CHEMICAL PESTICIDES

AND HERBICIDES IN CANADA
Early in 2002, Canada’s largest food distributor made a public
commitment to stop marketing chemical pesticides within a year,
by the beginning of the growing season in 2003. Loblaw Companies
Limited announced that it would no longer sell chemical pesticides
in its 440 garden centers. “In response to overwhelming consumer
Solutions 243
demand to eliminate the cosmetic use of pesticides in home gar-

dens, Loblaw Companies Limited has decided to discontinue the
sale of chemical pesticides in our garden centers, starting with the
spring season 2003,” said Loblaw spokesperson Geoff Wilson (“Gi-
ant Canadian” 2002).
The company timed its announcement to coincide with the March
14, 2002, opening of the annual Canada Blooms Flower and Garden
Show at the Metro Toronto Convention Centre, of which Loblaw is
the primary sponsor. “We will use this venue to launch our com-
mitment to Chemical Pesticide Free by 2003 and to further educate
gardeners on how they can enjoy a chemical pesticide-free garden,”
Wilson said (“Giant Canadian” 2002). According to Environment
Canada, a federal agency, homeowners use only 5 to 10 percent of
all pesticides sold in Canada, but they tend to use them inappro-
priately more often than commercial or agricultural users. The En-
vironment News Service reported that the agency advised Canadian
homeowners to keep the use of hazardous chemicals to a minimum.
The Sierra Club of Canada joined Loblaw in advising that many
pesticides cause damage to wild species. The Sierra Club said that
Carbofuran, a Canadian brand, was banned for most uses during
the late 1990s, after it was found to be responsible for the near-
extinction of the burrowing owl. “Evidence indicates that even the
family dog is a victim of pesticides. Dogs from homes with lawns
that have been sprayed with pesticides have a higher than average
rate of the canine equivalent of lymphoma. Cancer is now the num-
ber one cause of death in dogs,” the Sierra Club said (“Giant Ca-
nadian” 2002).
Loblaw Companies’ garden centers have carried some organic-
based gardening products in the past. Last year, the company ap-
proached its suppliers to develop more organic-based gardening
products to replace their chemical pesticides. “By the spring of
2003, we will have organic alternatives for virtually all of the chem-
ical pesticides that we currently carry,” Wilson said. Company staff
will provide educational handouts and information to consumers
on how they can reduce their dependency on chemical pesticides
(“Giant Canadian” 2002).
During 2001, according to the Environment News Service, the Su-
preme Court of Canada established a legal right for municipalities
to forbid the use of chemical pesticides on public and private prop-
erty within their jurisdictions. On June 28, 2001, the Supreme
244 The Dirty Dozen
Court upheld Bylaw 207 of the town of Hudson, Quebec, which bans
pesticide use on public and private property for aesthetic purposes.
The bylaw had been challenged in the Quebec courts and then in
the Canadian Supreme Court by lawn-pesticide companies after
they were charged with violating the ban (“Giant Canadian” 2002).
PHYTOREMEDIATION: PLANTS THAT ABSORB

HEAVY METALS AND ORGANIC CHEMICALS
Also during 2002, almost $2.22 million worth of grants was
awarded to seven universities to study the ability of plants to treat
soils contaminated by heavy metals or organic chemicals. The re-
search studied phytoremediation, which was described by the En-
vironment News Service as “The use of plants to degrade, remove or
stabilize toxic compounds from contaminated soil and water in ways
that are less expensive and less disruptive than traditional cleanup
techniques” (“$2.2 Million” 2002).
The U.S. EPA and the National Science Foundation sponsored the
grants to accelerate the development of innovative scientific solu-
tions to the worldwide problem of soil contamination by heavy met-
als and organic chemicals. Funding for the joint initiative was made
available through the Joint Program on Phytoremediation, a U.S.
federal government research effort involving the EPA, the National
Science Foundation, and the Departments of Defense and Energy.
Three grants were awarded through EPA’s Science to Achieve Re-
sults (STAR) program, designed to clarify the mechanism of phyto-
remediation of organic contaminants. These three grants were given
to the University of California, University of Connecticut, and Wash-
ington State University. The University of California at Riverside re-
ceived money to evaluate plant species that produce a specific group
of chemicals for use in phytoremediation and to study the ecology
of chemical-degrading bacteria that live in the root systems of these
plants. The University of Connecticut was funded to investigate the
role of plant roots in the phytoremediation of POPs in soil (“$2.2
Million” 2002). Washington State University will study the potential
use of spartina cordgrasses as a phytoremediation tool in marine
and estuarine sediments.
The National Science Foundation sponsored three multidisciplin-
ary research projects to investigate the genetic components of phy-
toremediation of heavy metals in soils. A grant went to Cornell
Solutions 245
University, one went to Purdue University, and a joint grant went

to Northwestern University and the University of Florida. Cornell
was funded to study the molecular basis for heavy-metal accumu-
lation and tolerance in one plant species. Purdue University at-
tempted to identify genes for metal accumulation in an entire plant
genome, the Brassicaceae family (“$2.2 Million” 2002). Northwest-
ern University and the University of Florida performed research to
clarify the mechanisms of arsenic uptake, translocation, distribu-
tion, and detoxification by brake ferns.
More information on these grants is available at http://www.
nsf.gov/bio/ibn/ibndevelop.htm and http://es.epa.gov/ncer/grants/
phyto01.html.
A TRUE GREEN OXIDANT

Scientists and the chemical industry have been testing new cat-
alytic oxidation systems that use metal complexes to break down
some POPs before they can pollute the atmosphere. Sayam Sen
Gupta and colleagues have reported in Science that a new oxidative
cleaning method may be useful in reducing pollution caused by
chlorinated phenols. The system uses hydrogen peroxide and iron
catalysts to eliminates between 90 and 98 percent of the offending
chemicals, without producing any other toxic by-products (Sen
Gupta et al. 2002; Meunier 2002). Much of the resulting mixture
(about 83 percent) is released as benign free chlorine. An analyst of
the process finds that it is much more efficient than biodegradation,
commenting that “An efficient catalytic chemical method for the ox-
idative degradation of chlorinated phenols, such as reported by Sen
Gupta, et al., is therefore highly welcome for treating industrial
wastewater before it is released” (Meunier 2002, 271). The nontoxic
nature of this process, according to Meunier, makes it a true green
oxidant.
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Glossary
Agent Orange: A dioxin-based defoliant (herbicide) widely used by the

United States during the Vietnam War.
Aldrin: An organochlorine pesticide; one of the dirty dozen to be banned
under the Stockholm Convention.
Anthropogenic: Caused or influenced by human activity.
Atrazine: Trade name of the most-often-used herbicide in United States ag-
riculture; it has been implicated in the demasculinization of male frogs
at concentrations as low as 1 ppb.
Biomagnification (also: bioaccumulation ): Increasing potency and toxicity of
POPs as they are consumed along a given food chain.
Cancer Alley: A nickname applied to a stretch of the Mississippi River be-
tween Baton Rouge and New Orleans, Louisiana, that includes several
mostly low-income, mainly African-American communities in the shad-
ows of petrochemical and plastics industries.
Carcinogenic: The propensity of a substance, such as an organochlorine
chemical, to cause cancer in humans or animals.
Chloracne: Small pimples with dark pigmentation of the exposed area, fol-
lowed by blackheads and pustules, induced by exposure to organochlo-
rine compounds.
Chlordane: An organochlorine pesticide; one of the dirty dozen to be banned
Chlorine: The basic chemical building block of the organochlorine chemical
family. It is the seventeenth element on the Periodic Table. Chlorine’s
powerful disinfectant qualities stem from its ability to bond with and de-
stroy the outer surfaces of bacteria and viruses.
Chlorofluorocarbons (CFCs): Organochlorine compounds widely used until
the 1990s (under the trade name Freon) in air conditioning and other
applications. During the 1980s, CFCs were found to be severely depleting
stratospheric ozone levels. These compounds were banned by an inter-
250 Glossary
national agreement (popularly known as the Montreal Protocol) negoti-

ated during the late 1980s, but they still are manufactured clandestinely
and smuggled by so-called Frio Banditos.
DDT (Para-dichlorodiphenyltrichloroethane): An organochlorine commonly
used as a pesticide; one of the dirty dozen to be banned under the Stock-
holm Convention.
Dibromochloropropane (DBCP): An organochlorine soil fumigant that has
caused infertility in men who have been exposed to the compound at their
work sites.
Dieldrin: an organochlorine commonly used as a pesticide; one of the dirty
dozen.
Diethylstilbestrol (DES): A form of synthetic estrogen that was given to at
least five million women to prevent miscarriages and pregnancy compli-
cations. The chemical was banned in 1971 after it was linked to increases
in a previously rare form of vaginal cancer.
Dioxins: A family of very toxic industrial chemicals to be banned under the
Stockholm Protocol as part of the dirty dozen.
Dirty dozen: The twelve most commonly used toxic POPs slated for inter-
national ban under the Stockholm Convention. See also Aldrin, Chlordane,
DDT, Dieldrin, Dioxins, Endrin, Furans, Heptachlor, Hexachlorobenzene,
Mirex, PCBs, and Toxaphene.
Dobson units: A measurement of atmospheric ozone levels, most notably in
the stratosphere.
Endocrine disrupter: A substance with the ability to interfere with hormone-
related functions in animals associated, at different levels of contamina-
tion, with several of the organochlorines.
Endrin: An organochlorine pesticide; one of the dirty dozen to be banned
Estrogen: A hormone that imparts feminine qualities.
Estrogen mimicry: The ability of organochlorine compounds to act with es-
trogenic properties in the bodies of humans and other animals and
thereby interfere with reproduction. Such an effect by DDT was reported
in chickens as early as 1950.
Frio Banditos: Smugglers of chlorofluorocarbons, notably Freon, usually
from Mexico into the United States.
Furans (a.k.a. polychlorinated dibenzofurans): Industrial chemicals to be
banned among the dirty dozen under the Stockholm Convention.
Global warming: The retention, near the Earth’s surface, of heat provoked
by rising levels, in the lower atmosphere, of heat-trapping trace gases,
such as carbon dioxide, methane, and some of the organochlorines.
Heptachlor: One of the dirty dozen.
Hexachlorobenzene: An organochlorine pesticide; one of the dirty dozen to
be banned under the Stockholm Convention.
Glossary 251
Intersex (also, imposex): Having reproductive organs of both sexes (usually

intersex), or secreting hormones of both sexes (usually imposex), a con-
dition that may be induced in some animals (most notably some fish spe-
cies and frogs) by exposure to organochlorine chemicals.
Love Canal: A neighborhood near Niagara Falls, New York, that was con-
taminated by a number of environmental toxic agents, including dioxins.
In 1978 President Jimmy Carter declared Love Canal a federal disaster
area, the first such declaration for a human-induced environmental
disaster.
Mercury Sunrise: The first sunrise of Arctic spring that initiates a series of
chemical reactions that dump mercury out of the atmosphere into the
polar snow pack, from which it is released into the food web during the
brief polar growing season. First reported in the Arctic during 1998.
Methyl bromide: A pesticide that is banned in several countries, including
the Netherlands and Canada, but allowed in the United States as of this
writing. This chemical may play a role in stratospheric ozone depletion.
Mirex: An organochlorine pesticide; one of the dirty dozen to be banned un-
der the Stockholm Convention.
Organochlorines: Chlorine-based chemicals. Organo, in this case, refers to
the presence of carbon in combination with chlorine.
Ozone: Three molecules of oxygen in combination that is depleted by chem-
ical interaction in the stratosphere by some organochlorines. Ozone ab-
sorbs ultraviolet radiation that would otherwise contribute to skin
cancers in human beings and other animals. See also Dobson units.
Ozone hole: Depletion of stratospheric ozone levels, notably over the Ant-
arctic and Arctic, by chlorofluorocarbons and other chemical processes.
The depletion does not form a hole in the ozone shield but depletes it to
a point that allows dangerous levels of ultraviolet radiation to reach the
surface.
Persistent organic pollutants (POPs): Carbon-based chemical compounds
and mixtures that share four characteristics: high toxicity, persistence,
a special affinity for fat, and a propensity to evaporate and travel long
distances. These chemicals have been commonly used as herbicides and
pesticides, or produced as by-products of several industrial processes, all
of which release toxicity into the environment.
Phytoremediation: The use of plants to absorb heavy metals and organic
chemicals.
Polar stratospheric clouds (PSCs): Earth’s highest clouds, which form above
the poles at altitudes of eighty-two to eighty-six kilometers. These clouds
have been increasing in coverage and thickness during the last four de-
cades, changes that may be linked to human emissions of carbon dioxide
and methane, as well as to depletion of stratospheric ozone. Until re-
cently, clouds at such heights were extremely rare.
252 Glossary
Polychlorinated biphenyls (PCBs): A family of industrial chemicals; included

among the dirty dozen to banned under the Stockholm Convention.
Polyvinyl chloride (PVC): A major constituent of many soft plastics, including
toys (such as Barbie dolls); a major source, in manufacture, of several
organochlorine pollutants, notably dioxins.
Precautionary principle: Developed at the Rio Earth Summit (1992), the pre-
cautionary principle holds that where there are threats of serious or ir-
reversible damage, lack of full scientific certainty shall not be used as a
reason for postponing cost-effective measures to prevent environmental
degradation. The chemical industry has long argued that harm should be
proven before products are removed, but environmentalists believe the
search for a largely unattainable degree of scientific certainty is a corpo-
rate stalling tactic.
Seveso, Italy: Site of a massive dioxin spill during 1976.
Silent Spring: Title of a well-known book by Rachel Carson, published in
1962, which raised widespread popular concern about the effects of or-
ganochlorines (most notably DDT) on the environment.
Sink: An area, such as the Arctic or Antarctic, to which organochlorine com-
pounds, most notably PCBs and dioxins, are carried by atmospheric and
oceanic currents and then deposited. The word is used by climate sci-
entists differently to indicate an area that absorbs carbon dioxide, as in
a “carbon sink.”
Sperm count: The number of motive (moving, or living) sperm in a given
volume of a man’s semen. Low sperm counts are said to be azoospermic
(having no sperm to count) and oligospermic (having sperm counts of less
than 20 million per milliliter).
Stockholm Convention: An international protocol that requires a ban of the
twelve most commonly used persistent organic pollutants (the dirty
dozen).
Times Beach, Missouri: A town that was contaminated by dioxins to a point
where it became uninhabitable. The U.S. EPA bought the town, moved
the residents out, and demolished its homes during 1983.
Toxaphene: One of the dirty dozen.
Ultraviolet (UV) radiation: Part of the sun’s energy that is filtered out, for the
most part, by stratospheric ozone. Depletion of ozone at this level allows
UV radiation to reach the Earth, where it may cause skin cancer and other
health problems. See also chlorofluorocarbons (CFCs).
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Index
Abortion, spontaneous, and PCBs, warming, 60–61; mammals and POPs,

180–81 generally, 136–37; mercury in, 68–69;
Agarwal, Anil, 152 stratospheric ozone, depletion, 69–71,
Agent Orange, 119, 237, 249; birth 84, 85, 86, 88–89, 100; thunderstorms,
deformities and, 26; children and, 27, 66; ultraviolet radiation, 70–71;
29–30; sexual dysfunction in men, volcanic aerosols and ozone loss,
208–9; use during Vietnam War, 24- 100–101
31, 174 Argentina, Newfoundland; U.S. Navy
Akeya, Alexander, 58 base, contamination of, 54
Akwesasne, Mohawk reservation, Armyworms, 157–58
111–16; derivation of name, 111; Arsenic standards, drinking water, 237
diseases and PCBs at, 113–15; fluoride Asbestos, clothing from, 1
poisoning of cattle at, 115–16; origins Atrazine, 143–46, 186–87, 249; banned
of, 111; PCB contamination at, 111–16 in European countries, 144; frogs and,
Aldrin, 15, 249 143–46; levels in Midwest U.S. water,
Alkylphenols, 213–14; health damage, 186
214; uses, 214 Austin, J., 83
Allen, Joe, 108 Auyuittuq National Park (Baffin Island),
Allergies, in the Arctic, 65 61
Alligators and POPs, 149–51 Avants, Liz, 122
Amato, Chris, 116 Ayotte, Pierre, 181, 182
American Cyanamid Corp., 158
American Library Association, chlorine- Bald eagles, POPs, 155; reproductive
free paper, 240–41 failure, 135
Animashaun, Kishi, 121 Barbie dolls, 221, 222
Anniston, Alabama, and PCBs, 235, 236 Basel Convention (1989), 233
Apopka, Lake, alligators and POPs, Beckman, Kimberlee, 148
149–51 Belgium, chickens, dioxins, and PCBs
Arctic, as sink for POPs, 4, 5, 15, 17, (1999), 38–40
47–56, 65, 136, 252; global warming Beluga whales, PCBs in, 138–39; toxicity
and, 57–68; hunting, and global and diseases, 139
292 Index
Benedict, Ernest, 115 Chlorinated hydrocarbons, 2

Bi, Bui Dinh, 30 Chlorination, of water, 187–88; cancer
Binder, Richard, 59 risk, 187; swimming pools, 187–88
Bioaccumulation (biomagnification), 2, Chlorine, 2, 249; as basis for POPs, 12;
17, 18, 50, 51, 53, 133, 136, 148, 153, as disinfectant, 22; history of, 22; pulp
155, 166, 168, 177, 249 and paper, 240, 241
Bisphenol A, 221, 222 Chlorine Chemistry Council (CCC),
Bliss, Russell, 32, 33 24–25, 37
Blue Whales: global warming and ozone Chlorine industry, payroll of, 24–25
depletion, 97–98; krill, depletion of, Chlorofluorocarbons (CFCs), 89, 90, 93,
98; population decline of, 98 98, 230, 249; “Frio Banditos,” 93–94;
Borenstein, Seth, 88 history of, 78–80; ozone depletion and,
Brasseur, Guy P., 78 77, 80; stratospheric cooling and,
Breast cancer, 172, 173, 209–10, 222; 77–78, 80, 81; Teflon, and, 82; uses of,
estrogen, synthetic, 209–10; increasing 79
incidence, 210 Chloroform, 187, 188
Breast milk, contamination of, 17, 47, 48, Chlorpyrifos (Dursban), 188–89; children
51, 166, 175, 178, 179–80, 200, 209 and, 188, 189; origin as nerve gas, 188;
Brody, Charlotte, 219 persistence, 188; uses, 188
Bromine, and stratospheric ozone Christy, John, 87
depletion, 79, 80, 81, 82, 95 Cicerone, Ralph J., 96
Burlington, H., 200 Clapp, Richard, 184
Bush, George W., “sound science,” 57; Cocking, Dennis, 190
Stockholm Convention, and, 5, 8, 229, Colborn, Theodora, 17, 36–37, 148, 149,
230, 232 200, 202, 212
Butchart, N., 83 Cornell University Press, chlorine-free
paper, 240
Canada: toxic wastes, 124–25; U.S. Costner, Pat, 34, 152, 153, 201
military and, 124 Covenant, Louisiana, 118, 119, 120, 121
“Cancer Alley,” Louisiana, 117–124, 249; Cray, Charlie, 117
dioxin levels, 121–24; PVC levels, Crutzen, Paul, 82, 89, 102
119–20
Cancer rates, 172–74, 209–10; non- Dai, Le Cao, 31
Hodgkin’s lymphoma, 174 Darwin, Charles, 22
Cantrell, Chris, 97 Davy, Sir Humphrey, 22
Card, P.Q., 1 DDT, 5, 7, 8, 14, 35, 36, 126, 156, 165,
Carpenter, David, 113 250; bald eagles, 135, 155; estrogen
Carson, Rachel (Silent Spring, 1962), 3, mimicry and, 23, 24, 200; in fish, 169;
5, 6, 7, 8, 24, 36, 152, 155, 156, 165, in frogs, 142; Inuit mothers’ milk and,
252 52; malaria and, 230, 231;
Cau, Hoang Dinh, 30 manufactured in India, 128; in meat,
Chapman, Stuart, 98 20, 21; Stockholm Convention, 229,
Chemicals, lack of testing, 13 230, 231; in tea and coffee, 21;
Chevron Corp., 79 thinning eggshells and, 23, 24;
Children and POPs, 174–79, 180 vultures, India, 152–53
Chinjila, Mellon, 126, 127 DEW (Distant Early Warning) Line, and
Chloracne, origins, 23 PCBs, 53, 54, 55
Chlordane, 14 Dewailly, Eric, 15, 181
Index 293
Diazinon, 174 Endosulfan, in India, 189; effects on

Dibromochloropropane (DBCP), 207–9, children, 189; use on cashews, 189
250; Costa Rica, 208; infertility, in Endrin, 14, 250
men, 207–9; uses, 207–8 Environmental Protection Agency (U.S.):
Dieldrin, 14, 210, 250 conflicts of interest, 237–38; industry
Diethylstilbestrol (DES), 211–13, 221, and, 237, 238; review procedures,
250; cervical cancer, 212; dieting, and, 237–38
181–82; history, 212; infertility, 212; Epstein, Samuel S., 219
uses, 212; vaginal cancer, 211 Eskes, Henk, 102
Dioxins, 2, 12, 14, 15, 134, 140–41, Estrogen mimicry, 23, 24, 154, 155, 156,
182–84, 206, 207, 210, 237, 241, 250; 157, 200, 202, 203, 207, 209, 210, 221,
Agent Orange, as active ingredient, 25; 222, 250; Barbie dolls and, 221; DES,
Belgium, in chickens (1999), 38–40; 200; fish, 139–41; frogs, 141–42;
breastmilk, 175–76; “Cancer Alley,” heated plastic and, 221–22; noted in
Louisiana, 121–24; cancers and, 27, 28, 1930s, 23; prostate cancer, 213;
173–74, 183–84; children and, 177–78; research needed, 222
decline in levels, 183; fetal Estrogen, synthetic, 221, 250; breast
development and, 17; health maladies cancer, 209–10; DES, 211–13
attributed to, 28–30, 183; Love Canal, Ethanol, 191
New York, 32–33; male reproductive Ethyl Corp., 215
system, 208–9; natural defenses
against, 17; potency of, 3, 49; PVCs Fahey, David W., 91, 92, 93
and, 214–17; sex ratios, 210–11; sexual Feldman, David, 221
dysfunction and, 183; sources and uses Fetal development and POPs, 48, 135,
of, 182–83; spill, Seveso, Italy (1976), 154, 155, 168, 183, 200, 201, 202, 206
31–32; Times Beach, Missouri, 33–34; Fish, POPs and, 20, 21, 22, 167, 168–70,
toxic effects on wildlife, 133–58; 177
Vietnam, levels in, 28–30 Fluoride poisoning of cattle, Akwesasne,
“Dirty Dozen,” the, 4, 8, 250; listed, 115–16
13–15; Stockholm Convention, 229, Fogra Co. (Belgium), 38, 39
230, 231 Food, and POPs, 18–22
Dodds, E.C., 210 Foster, Mike, 122
Dosage levels, and toxicity, 167–68 Freon, 78; “Frio Banditos,” 93–94, 242,
Dow Chemical Corp., 217 250; smuggling of, 93–94
Drdla, Katja, 77 Frobisher, Martin, 58
“Drunken forest,” Alaska, 65 Frogs, and POPs, 141–43; Atrazine, and,
DuPont Chemical Corp., 78, 79 143–46; death rate and water acidity,
Dursban (Chlorpyrifos), 188–89; children 142; deformities, 141, 142; species
and, 188, 189; origin as nerve gas, 188; extinctions, 141
persistence, 188; uses, 188 Fry, Michael, 156
Furans, 14, 174, 250
Ebinghaus, Ralf, 69
Edgar, Linda Carol, 213 Gammon, Marilie, 173
Einspar, Ed, 110 Gardiner, David, 145, 146
Endocrine system, and POPs, 48, General Electric Co., 23, 34, 35
134.135, 199, 200–201, 202, 222; General Motors Corp., 112, 113, 114,
chemicals listed, 202 116
Endometriosis and POPs, 146, 147 General, Rowena, 114–15
294 Index
Georgia Gulf Corp., 118 Inuit, and POPs exposure, 16, 47–57,
Georgia Pacific Corp., 118 119, 176, 182
“Gift waste,” 125–27, 231; Tanzania and, Inuit infants, and POPs, 51; hearing loss,
125 51–53; hunting, in Arctic, effect on,
Global warming, 57–58, 59–68, 230, 250; 60–61; immune system weakness,
Arctic, 59–68; boreal forests and, 59, 52–53; mothers’ milk, 52
60; caribou and, 64, 65, 67, 68; Inuvik, record temperature at, 59
“drunken forest,” Alaska, 65; forecasts Iqaluit, Baffin Island, town dump and
of temperature rise, 67–68; glaciers POPs, 50–51
receding in Alaska, 62, 64; permafrost
and, 59; sea-ice cycles and, 60, 61, 64; Japan, pesticide use, 24
seals and, 66; Shishmaref, Alaska, Jayaraman, Nityanand, 127
erosion, 63–64; stratosphere, cooling Jock, Ken, 114
of, 84–88; thinning sea ice, 67; Johnston, Paul, 12
thunderstorms in the Arctic, 66
Goodrich, B.F. Corp., 215, 216 Kathpal, T.S., 152
Goulden, M.L., 59 Kendall, Ronald, 146
Graham, John, 237 Kerr, Richard, 91
Grant Chemical Co., 212 Kiesecker, Joseph, 144, 145
“Grasshopper effect,” 15 King, Jack, 192
Great Lakes, contamination of, 36, 148, Kirby, Jane, 108, 109
168, 169 Klose, Chris, 186–87
Greenpeace, 118, 119, 120, 122, 232, 236, Kooneeliusie, Steven, 60, 61
237 Krill, depletion of, 98
Guillette, Louis, 144, 150 Krimsky, Sheldon, 200, 212
Gulls and POPs, 156 Kuptana, Rosemarie, 65, 66
Halowax Corp., 23 Lake Trout, 149

Haraguchi, Koichi, 153 Landrigan, Philip, 5, 172
Hartmann, Dennis L., 87 Lazaroff, Cat, 217
Hayes, Tyrone B., 144 Lindane, 185–86; as endocrine disrupter,
Heptachlor, 14, 250 186; toxicity, 185–86; uses of, 185
Herbst, Arthur, 212 Lindberg, Steve E., 68, 69
Herman, Jack, 109, 110 Linderman, V.F. 200
Hexachlorobenzene, 14, 250 Loblaw Corp., 242–43
Hill, Geoffrey E., 158 Loch-Caruso, Rita, 180
Himes, Barry, 94 Long, Craig, 102
Hipskind, Steve, 70, 71 Love Canal, New York, 32, 251
HIV/AIDS, 171–72 Lynch, Elisa, 192
Hudson Bay, 60
Humphrey, Harold, 168 Malathion, 108–11, 157
Hunter-Cevera, Jennie, 242 Maltoni, Cesare, 216
Hydroxyl radicals, 95–97 Mann, Barbara Alice, 165
Mason, Dick, 120
I.G. Farben, 188 McClain, Mildred Bahati, 128–29
Immune systems and POPs, 134–35, McConnell, Jack, 98
139, 170–72, 179, 202 McElroy, Tom, 99
Imposex, 251 Melancon, Patricia, 121
Intersex, 150–51, 251 Mercury, in the Arctic, 68–69
Index 295
“Mercury sunrise,” 68–69, 251 22–25; number of, 5, 7; pervasiveness,

Methane, 98, 99 11, 12; production of, history, 5–6
Methane oxidation, stratospheric, 78 Osorno, Lidia Amarales, 103
Methyl bromide, 251; ozone depletion Ozone, stratospheric, 251; depletion of,
and, 95; toxicity of, 94–95 79, 81, 82, 86–88, 89, 92–93, 100, 251;
Methyl tertiary butyl ether (MTBE), depletion of, over Arctic, 69–71;
189–92; ban of, California, 192; methyl bromide, and 94–95
gasoline additive, 189; groundwater
contamination by, 190–92; lack of Panoor, Tim, 144
testing, 189; leaks of, 191; legal Panthers and POPs, 151
actions, 192; levels, by city, 191; uses Paruk, Brian, 61
of, 190 Penjueli, Maureen, 220
Mexico, children and POPs, 178 Persistent organic pollutants (POPs), 2,
Midgerly, Thomas, 78, 79 251; alligators and, 149–51;
Millam, James, 157 armyworms, 157–58; bald eagles and,
Mirex, 14, 251 155; biomagnification of, 2–3; cancer
Mission, South Dakota, 108–11 rates, 172–74; catalytic breakdown,
Mocarelli, Paolo, 210–11 245; characteristics of, 11; children
Molina, Mario, 79, 80 and, 174–79; continuing presence of,
Monkeys, abortions, 155 232; declining sperm counts and, 6–7;
Monsanto Corp., 174, 235 defined, 11; dieting and, 181–82;
Montague, Peter, 142, 146, 147, 234 disease and, in humans, 168; dogs,
Montreal Protocol, 70, 230, 242 cancer in, 243; dosage levels, and
Montzka, Stephen A., 96 toxicity, 167–68; endometriosis and,
Mossville, Louisiana, dioxin levels at, 146, 147; farm workers and, 16; fetal
122 development and, 48; fish, 52, 167,
Moyers, Bill, “Trade Secrets,” 123, 215, 168–70; food, 18–22, 175; fur seals
216 and, 148; global pollution by, 16; Great
Musil, Robert, 233 Lakes, 148–49; gulls, 156; history of,
22–25; HIV/AIDS, 171–72; immune
systems and, 134–35, 139, 170–72;
Nakoolak, Solomon, 61
Inuit infants and, 52; Lake Trout, 148;
Napier, Robert, 173
levels of toxicity, 17; mobility, 15;
Nayokpuk, Percy, 63
monkeys and, 155; mothers’ milk and,
Netting, Jessa, 141
52; panthers and, 151; persistence of
Newman, Paul, 89, 92
toxicity, 8, 15; polar bears and, 3, 52;
Nitrous oxide, 98, 99
production of, by state, 178; safety
Non-Hodgkin’s lymphoma, 174
standards, food, 21; seals and, 148;
Norilsk, Russia, nickel smelter
soluble in fat, 2, 16, 17; South Asia
contamination, 55
and, 127–28; Stockholm Convention,
Northwest Passage, 58
229, 230, 231; toxicological effects, 6;
Nunavut, 47; socioeconomic changes,
undescended testicles and, 146;
56–57
vultures and, 152–53; whales and, 52,
153–54; worldwide pollution via, 1–2,
Olea, Nicholas, 222 132–33; zebra finches and, 157
Olson, Erik, 237 Pesticides: expenditures on, 6; global
O’Neill, Alan, 90 production of, 13; increasing potency
“Operation Ranch Hand,” 26 of, 13; lack of testing on, 8
Organochlorines, 2, 251; history of, Pharmacia Corp., 235
296 Index
Phthalates, 176–77, 213–14, 217–20; Qamanakiq, Simon, 62

health damage, 214; uses of, 214, Qitsualik, Rachel Attituq, 57
217–19
Phytoremediation, 244–45, 251
Ransom, James, 113
Pine Bluff (Arkansas) Arsenal, 107, 108
Rats, feminized by POPs, 134
Polar bears, and POPs, 3, 47–48, 136–37;
Reindeer, heavy metals and, 137–38
Churchill, Manitoba, 62; and global
Reinjders, Per, 149
warming, 61–62, 65; reproductive
Reproductive abnormalities and POPs,
failure, 136–37; weight declines, 62
167, 199, 200–201, 205–9; alligators,
Polar stratospheric clouds (PSCs), 251;
149–51; fish, 139–41; fur seals, 148;
ozone depletion and, 82, 83, 91, 92,
humans, 199, 200–201; panthers, 151;
93, 100
wildlife, 36–37
Pollution, world-wide character, 1–2, 133
Reymert, Per Kyrre, 137
Polychlorinated biphenyls (PCBs), 2, 12,
Reynolds, Ray, 123
14, 15, 20, 231, 241, 252; Akwesasne
Rhee, Donna, 187
(Mohawk Reservation) and, 111–16;
Rice oil contamination, 170, 207; Japan,
Argentina, Newfoundland, 54;
170; Taiwan, 170, 207
bacterium degrades, 241–42; Belgium,
Rosebud Sioux, 108–11
in chickens, 38–40; children and, 177,
Ross, Dan, 123, 216–17
200; diseases at Akwesasne and,
Rowland, Sherwood, 79, 80, 91, 96
113–15; fire suppression and, 22, 23;
fish, 177; Hudson River, New York,
34–35; levels of toxicity, 17; mink Sach’s Harbour, Banks Island, 65–66
extinction, 134; otter population Saint Lawrence Seaway, 112
declines, 134; U.S. military bases in Salawitch, Ross, 89
Canada and, 124 Salter, Elizabeth, 137
Polyvinyl chlorides (PVCs), 117, 118, Santee, Michelle, 90
119, 207, 252; abortion, spontaneous, Santillo, David, 19
180–81; ban proposed, 236–37; Barbie Schecter, Arnold O., 29
dolls, 221; breast milk and, 175–76, Scheele, Carl Wilhelm, 22
179–80; “Cancer Alley,” Louisiana, Schettler, Ted, 175, 179, 209
119–20, 123; childhood and, 166–67; Scott, Peter, 60
dioxins and, 117, 214–15, 217, 236–37; Seals and POPs, 47, 48, 148
diseases and, 119, 120; European ban Seinfeld, John H., 97
of, 220; fetal exposure, 166–67; fish Sen Gupta, Sayam, 245
consumption and, 166–70; history of, Seveso, Italy, dioxin spill (1976), 31–32,
215–16; HIV/AIDS, 171–72; PCBs and, 210–11
217; plastics from, 214–17; production Sex ratios, 210–11
of, 13, 215; uses, 214; Zambia, rustling Sexual development, and POPs, 199;
of, 125–27 alligators, 149–51; disruption by POPs,
Precautionary principle, 235, 252 133–35; frogs, and POPs, 143–46
Prinn, Ronald G., 95, 97 Shanklin, Jonathan, 84, 85
Project SOLVE, 88–90 Shashoua, Yvonne, 221
Proof, problems with, 234–35 Shell Oil Corp., 192
Prostate cancer, estrogen mimics and, 213 Sherwood, Steven, 99
Pungowiyi, Caleb, 58 Shindell, Drew, 84, 86, 91
Punta Arenas, Chile, ozone-depletion Shine, K.P., 83
warnings at, 102–3 Shintech Corp., 118, 119, 120, 121, 122
Index 297
Shishmaref, Alaska, eroding into ocean, Tosco Corp., 192

63–64 Toxaphene, 15, 252
Sierra Club of Canada, 243 Toxic wastes: Canada, 124–25;
Silver, Larry B., 179 concentrations in poor communities,
Singh, Jagdish Prasad, 152 107–8, 128–29; volume of, world-wide,
Skekkebaek, Niels: declines, human 166
sperm counts, 148, 203, 204; testicular “Toxics Patrol,” Greenpeace, 118, 122
cancer studies, 148 Tuktoyaktuk (village), 58, 59, 64
Solutia Corp., 235 Tyler, Michael J., 142
South Asia, and POPs, 127–28
Spencer, Roy, 87 Ultraviolet radiation, 70–71, 99, 252;
Sperm counts, 199, 200, 201, 203–5, 208, effects of, 78; northern hemisphere, 88
213, 252; humans, 148, 151, 200, 201, Undescended testicles and POPs, 146,
203–5, 208; lower counts in rural 206, 213
areas, 205; POPs and, 204–5; rats, 154, Union Carbide Corp., 216
206 United States of America, pesticide use, 24
Spitzer, Eliot, 116 Uranium, mined by Navajos, 1
Squillace, Paul, 191
Stockholm Convention, on POPs, 5, 8,
15, 229–31, 252; DDT, exception Verkest Co. (Belgium), 38, 39
under, 229, 230, 231; POPs, terms of Versele Co. (Belgium), 38, 40
elimination, 229–30 Vinclozolin, 146
Stratospheric ozone: CFCs, and depletion Viola, P.L., 216
of, 77, 78, 80, 81; cooling and global Vom Saal, Frederick, 18
warming, 78; denitrification and Vultures, India, 152–53
depletion of, 91; depletion of, 77, 78,
92, 93, 98, 99, 100; projections of Watt-Cloutier, Sheila, 47, 49, 53, 55
recovery, 90–91; volcanic aerosols and Waxman, Henry A., 237
ozone loss, 100–101 Webb, Jeremy, 97
Sumpter, John, 139, 140 Weiss, Ray F., 96
Swan, Shanna, 205 Welch, Harold, 66–67
Syngenta Corp., 144, 146 Weller, Gunter, 60, 64
Weybridge Report, 146, 201, 234, 235
Weyiouanna, Clifford, 63
Tabazadeh, Azadeh, 91, 95, 99, 100 Weyiouanna, Edwin, 64
Tanzania, and “gift waste,” 125 Whales, and POP toxicity, 153–54
Testicular cancer, 201, 203, 205–6 Wildlife, and POP toxicity, 133–58
Thin Elk, Anna Carol, 109–10 Wilkin, Dwane, 57
Thoa, Nguyen Kim, 29–30 Wilson, Geoff, 243
Thompson, Dana Leigh, 112 Windsor, Clifford, 242
Thompson, Loren, 116 Wingspread Conference (1991), 37
Thompson, Paul, 112, 114 Wise, Jeff, 178
Thornton, Joe, 5, 171, 173, 215
Times Beach, Missouri, dioxin
contamination, 33–34, 170, 252 York, Geoffrey, 55
Toluene, 184–85
Toolie, Jimmy, 58 Zambia, PCB rustling, 126–27
Toon, Brian, 88 Zebra finches and POPs, 157
About the Author
BRUCE E. JOHANSEN is Robert T. Reilly Professor of Communi-

cation and Native American Studies at the University of Nebraska
at Omaha. His last book was The Ecocide of Native America (1995).

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THE DIRTY DOZEN:

Toxic Chemicals and

Johansen, Bruce E. (Bruce Elliott), 1950–

British Library Cataloguing in Publication Data is available.

Copyright 䉷 2003 by Bruce E. Johansen

All rights reserved. No portion of this book may be

Library of Congress Catalog Card Number: 2002029872

First published in 2003

Praeger Publishers, 88 Post Road West, Westport, CT 06881

Printed in the United States of America

The paper used in this book complies with the

1. Persistent Organic Pollutants: The Basics 11

I was introduced to the human and natural toll of persistent organic

negotiated are the methods and pace of their elimination, ﬁrst in

Our economic system has been very good at developing ways to

chlorinated hydrocarbons that have left a devastating environmen-

small levels of such contaminants in water or soil can magnify into

Every human being is now subjected to contact with dangerous chemicals,

During the early twentieth century, human beings learned to syn-

The Dirty Dozen begins in chapter 1 with a basic primer on syn-

Chapter 8 surveys public-policy solutions to the POP dilemma.

It makes no sense to presume that the thousands of organochlorines not

Synthetic organochlorines are created by combining the mole-

At least 11,000 organochlorines are produced commercially. Many thou-

Expenditures on pesticides in the United States, in constant 1996

counts, fetal malformations, neurobehavioral impairment, and

I contend, therefore, that we have allowed these chemicals to be used with

Agencies concerned with vector-borne disease are at present coping with

Two present-day observers note that the register of potentially

mental and ecotoxicological properties of such substances are even more

Carson wrote only a decade and a half after organochlorines be-

Commercial organochlorines have become pervasive in our every-

middle of the Paciﬁc. Penguins in Antarctica have been found to be

Heat-resistant PCBs became standard liquid insulation in elec-

ilarly hazardous properties continue to be used and released to the

Several of these synthetic chemicals (including PCBs and dioxins,

THE PERSISTENCE AND MOBILITY OF POPS

The pollution of PCBs (among other organochlorines) is truly

DISSENTERS TO THE MAJORITY PARADIGM

Lakes wildlife, Theo Colborn found that microscopic organisms pick

A Greenpeace report published in March 2000 warned that much

cessive intake of dioxins in U[nited] K[ingdom] children” (Santillo

proportion of milk in calves’ diets. In India, a high proportion of

A BRIEF HISTORY OF POPS

stucco. They found many uses in varnishes, inks, and paints, as

The Swan Chemical Corp. (later a division of Monsanto) had be-

had in the neighborhood of 50 to 60 men afﬂicted with various degrees of

As early as the 1930s, tests of laboratory animals revealed estro-

throughout the environment; he found it even in hair samples taken

AGENT ORANGE IN VIETNAM

Saigon, now Ho Chi Minh City, increased tenfold between 1954

do not prove dioxin causes diabetes, only that there appears to be

poster. A reporter described Thoa’s delicate features, “wrapped in a

nam should not be blamed wholesale on Agent Orange, and may be

DIOXIN SPILL AT SEVESO, ITALY (1976)

LOVE CANAL BECOMES A TOXICOLOGICAL

TIMES BEACH, MISSOURI, CEASES TO EXIST

and lodging, perhaps, eventually in the milk of an Inuit mother, or

A SUPERFUND SITE ON THE HUDSON

haul thousands of pounds of the foul-smelling stuff to presumably distant

Before the EPA order, GE ofﬁcials spent at least $15 million on an

OPPOSITION TO POPS GALVANIZES